請用此 Handle URI 來引用此文件：
http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/81028完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 郭靜穎(Ching-Ying Kuo) | |
| dc.contributor.author | Ge-Jyun Liu | en |
| dc.contributor.author | 劉格均 | zh_TW |
| dc.date.accessioned | 2022-11-24T03:26:53Z | - |
| dc.date.available | 2021-09-16 | |
| dc.date.available | 2022-11-24T03:26:53Z | - |
| dc.date.copyright | 2021-09-16 | |
| dc.date.issued | 2021 | |
| dc.date.submitted | 2021-08-30 | |
| dc.identifier.citation | 1. 衛生福利統計部，109年死因統計結果分析https://eysc.ey.gov.tw/Page/3661BDDEE464D3C8/610b1b81-de20-4b52-9dc9-236224c0d260 2. Sung, Hyuna, et al. 'Global cancer statistics 2020: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries.' CA: a cancer journal for clinicians 71.3 (2021): 209-249. 3. Bray, F. et al. Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA: A Cancer J. Clin. 68, 394–424. 4. Shen, Jing, et al. 'Dependence of cancer risk from environmental exposures on underlying genetic susceptibility: an illustration with polycyclic aromatic hydrocarbons and breast cancer.' British journal of cancer 116.9 (2017): 1229-1233. 5. Huang, Chiun-Sheng, et al. 'Unique features of breast cancer in Asian women—breast cancer in Taiwan as an example.' The Journal of steroid biochemistry and molecular biology 118.4-5 (2010): 300-303. 6. Wu, Hui-Chen, et al. 'Reproductive and environmental exposures and the breast cancer risk in Taiwanese women.' Scientific Reports 11.1 (2021): 1-7. 7. Miller, Kimberly D., et al. 'Cancer treatment and survivorship statistics, 2019.' CA: a cancer journal for clinicians 69.5 (2019): 363-385. 8. Nielsen, Torsten O., et al. 'Immunohistochemical and clinical characterization of the basal-like subtype of invasive breast carcinoma.' Clinical cancer research 10.16 (2004): 5367-5374. 9. Rivenbark, Ashley G., Siobhan M. O’Connor, and William B. Coleman. 'Molecular and cellular heterogeneity in breast cancer: challenges for personalized medicine.' The American journal of pathology 183.4 (2013): 1113-1124. 10. Heimes, Anne-Sophie, and Marcus Schmidt. 'Atezolizumab for the treatment of triple-negative breast cancer.' Expert opinion on investigational drugs 28.1 (2019): 1-5. 11. Mavratzas, Athanasios, et al. 'Atezolizumab for use in PD-L1-positive unresectable, locally advanced or metastatic triple-negative breast cancer.' Future oncology 16.3 (2020): 4439-4453. 12. Schmid, Peter, et al. 'Atezolizumab and nab-paclitaxel in advanced triple-negative breast cancer.' New England Journal of Medicine 379.22 (2018): 2108-2121. 13. FDA approves atezolizumab for PD-L1 positive unresectable locally advanced or metastatic triple-negative breast cancer | FDA. [Online] (2019). https://www.fda.gov/drugs/drug-approvals-and-databases/fda-approves-atezolizumab-pd-l1-positive-unresectable-locally-advanced-or-metastatic-triple-negative. Accessed 18 Nov 2020 14. FDA grants accelerated approval to pembrolizumab for locally recurrent unresectable or metastatic triple negative breast cancer | FDA. [Online] (2020). https://www.fda.gov/drugs/drug-approvals-and-databases/fda-grants-accelerated-approval-pembrolizumab-locally-recurrent-unresectable-or-metastatic-triple. Accessed 17 Nov 2020 15. Starodub, Alexander N., et al. 'First-in-human trial of a novel anti-Trop-2 antibody-SN-38 conjugate, sacituzumab govitecan, for the treatment of diverse metastatic solid tumors.' Clinical Cancer Research 21.17 (2015): 3870-3878. 16. Goldenberg, David M., Rhona Stein, and Robert M. Sharkey. 'The emergence of trophoblast cell-surface antigen 2 (TROP-2) as a novel cancer target.' Oncotarget 9.48 (2018): 28989. 17. Ambrogi, Federico, et al. 'Trop-2 is a determinant of breast cancer survival.' PloS one 9.5 (2014): e96993. 18. Ocean, Allyson J., et al. 'Sacituzumab govitecan (IMMU‐132), an anti‐Trop‐2‐SN‐38 antibody‐drug conjugate for the treatment of diverse epithelial cancers: Safety and pharmacokinetics.' Cancer 123.19 (2017): 3843-3854. 19. Seligson, John M., et al. 'Sacituzumab Govitecan-hziy: An antibody-drug conjugate for the treatment of refractory, metastatic, triple-negative breast cancer.' Annals of Pharmacotherapy 55.7 (2021): 921-931. 20. FDA grants accelerated approAval to sacituzumab govitecan-hziy for metastatic triple negative breast cancer | FDA. [Online] (2020). https://www.fda.gov/drugs/resources-information-approved-drugs/fda-grants-accelerated-approval-sacituzumab-govitecan-hziy-metastatic-triple-negative-breast-cancer. Accessed 22 April 2020 21. Allemani, Claudia, et al. 'Global surveillance of trends in cancer survival 2000–14 (CONCORD-3): analysis of individual records for 37 513 025 patients diagnosed with one of 18 cancers from 322 population-based registries in 71 countries.' The Lancet 391.10125 (2018): 1023-1075. 22. Cancer Genome Atlas Network. 'Comprehensive molecular portraits of human breast tumours.' Nature 490.7418 (2012): 61. 23. Gonzalez-Angulo, Ana Maria, Flavia Morales-Vasquez, and Gabriel N. Hortobagyi. 'Overview of resistance to systemic therapy in patients with breast cancer.' Breast cancer chemosensitivity (2007): 1-22. 24. Gandhi, Nishant, and Gokul M. Das. 'Metabolic reprogramming in breast cancer and its therapeutic implications.' Cells 8.2 (2019): 89. 25. Reid, Michael A., and Mei Kong. 'Dealing with hunger: Metabolic stress responses in tumors.' Journal of carcinogenesis 12 (2013). 26. Hay, Nissim. 'Reprogramming glucose metabolism in cancer: can it be exploited for cancer therapy?.' Nature Reviews Cancer 16.10 (2016): 635. 27. Vander Heiden, Matthew G., Lewis C. Cantley, and Craig B. Thompson. 'Understanding the Warburg effect: the metabolic requirements of cell proliferation.' science 324.5930 (2009): 1029-1033. 28. Helmlinger, Gabriel, et al. 'Interstitial pH and pO2 gradients in solid tumors in vivo: high-resolution measurements reveal a lack of correlation.' Nature medicine 3.2 (1997): 177-182. 29. Vincent, Emma E., et al. 'Mitochondrial phosphoenolpyruvate carboxykinase regulates metabolic adaptation and enables glucose-independent tumor growth.' Molecular cell 60.2 (2015): 195-207. 30. Pan, Min, et al. 'Regional glutamine deficiency in tumours promotes dedifferentiation through inhibition of histone demethylation.' Nature cell biology 18.10 (2016): 1090-1101. 31. Reid, Michael A., et al. 'The B55α subunit of PP2A drives a p53-dependent metabolic adaptation to glutamine deprivation.' Molecular cell 50.2 (2013): 200-211. 32. Al Tameemi, Wafaa, et al. 'Hypoxia-modified cancer cell metabolism.' Frontiers in cell and developmental biology 7 (2019): 4. 33. Majmundar, Amar J., Waihay J. Wong, and M. Celeste Simon. 'Hypoxia-inducible factors and the response to hypoxic stress.' Molecular cell 40.2 (2010): 294-309. 34. Semenza, Gregg L. 'Defining the role of hypoxia-inducible factor 1 in cancer biology and therapeutics.' Oncogene 29.5 (2010): 625-634. 35. Pakos‐Zebrucka, Karolina, et al. 'The integrated stress response.' EMBO reports 17.10 (2016): 1374-1395. 36. Harding, Heather P., et al. 'An integrated stress response regulates amino acid metabolism and resistance to oxidative stress.' Molecular cell 11.3 (2003): 619-633. 37. Gao, Song, et al. 'PSAT1 is regulated by ATF4 and enhances cell proliferation via the GSK3β/β-catenin/cyclin D1 signaling pathway in ER-negative breast cancer.' Journal of Experimental Clinical Cancer Research 36.1 (2017): 1-13. 38. Baird, Liam, and Albena T. Dinkova-Kostova. 'The cytoprotective role of the Keap1–Nrf2 pathway.' Archives of toxicology 85.4 (2011): 241-272. 39. Kansanen, Emilia, et al. 'The Keap1-Nrf2 pathway: Mechanisms of activation and dysregulation in cancer.' Redox biology 1.1 (2013): 45-49. 40. Ma, Qiang. 'Role of nrf2 in oxidative stress and toxicity.' Annual review of pharmacology and toxicology 53 (2013): 401-426. 41. Galadari, Sehamuddin, et al. 'Reactive oxygen species and cancer paradox: to promote or to suppress?.' Free Radical Biology and Medicine 104 (2017): 144-164. 42. Zorov, Dmitry B., Magdalena Juhaszova, and Steven J. Sollott. 'Mitochondrial reactive oxygen species (ROS) and ROS-induced ROS release.' Physiological reviews 94.3 (2014): 909-950. 43. Panieri, E., and M. M. Santoro. 'ROS homeostasis and metabolism: a dangerous liason in cancer cells.' Cell death disease 7.6 (2016): e2253-e2253. 44. Zhao, Yang, et al. 'ROS signaling under metabolic stress: cross-talk between AMPK and AKT pathway.' Molecular cancer 16.1 (2017): 1-12. 45. Chaube, Balkrishna, et al. 'AMPK maintains energy homeostasis and survival in cancer cells via regulating p38/PGC-1 α-mediated mitochondrial biogenesis.' Cell death discovery 1.1 (2015): 1-11. 46. Murphy, Michael P. 'How mitochondria produce reactive oxygen species.' Biochemical journal 417.1 (2009): 1-13. 47. Fruman, David A., et al. 'The PI3K pathway in human disease.' Cell 170.4 (2017): 605-635. 48. Elstrom, Rebecca L., et al. 'Akt stimulates aerobic glycolysis in cancer cells.' Cancer research 64.11 (2004): 3892-3899. 49. Nogueira, Veronique, et al. 'Akt determines replicative senescence and oxidative or oncogenic premature senescence and sensitizes cells to oxidative apoptosis.' Cancer cell 14.6 (2008): 458-470. 50. Go, Christina K., et al. 'EGR-mediated control of STIM expression and function.' Cell calcium 77 (2019): 58-67. 51. Hao, Leiyu, et al. 'The Role of Early Growth Response Family Members 1–4 in Prognostic Value of Breast Cancer.' Frontiers in Genetics 12 (2021): 809. 52. Unoki, Motoko, and Yusuke Nakamura. 'EGR2 induces apoptosis in various cancer cell lines by direct transactivation of BNIP3L and BAK.' Oncogene 22.14 (2003): 2172-2185. 53. Wu, Qiong, et al. 'MiR-150 promotes gastric cancer proliferation by negatively regulating the pro-apoptotic gene EGR2.' Biochemical and biophysical research communications 392.3 (2010): 340-345. 54. Zhang, Shujuan, et al. 'Early growth response 3 inhibits growth of hepatocellular carcinoma cells via upregulation of Fas ligand.' International journal of oncology 50.3 (2017): 805-814. 55. Shin, Seung-Hyun, et al. 'Loss of EGR3 is an independent risk factor for metastatic progression in prostate cancer.' Oncogene 39.36 (2020): 5839-5854. 56. Liao, Fei, et al. 'Decreased EGR3 expression is related to poor prognosis in patients with gastric cancer.' Journal of molecular histology 44.4 (2013): 463-468. 57. Matsuo, Taisuke, et al. 'Early growth response 4 is involved in cell proliferation of small cell lung cancer through transcriptional activation of its downstream genes.' PLoS One 9.11 (2014): e113606. 58. He, Susu, et al. 'A positive feedback loop between ZNF205‐AS1 and EGR4 promotes non‐small cell lung cancer growth.' Journal of cellular and molecular medicine 23.2 (2019): 1495-1508. 59. Gong, Xiaoli, et al. 'Gramicidin inhibits cholangiocarcinoma cell growth by suppressing EGR4.' Artificial cells, nanomedicine, and biotechnology 48.1 (2020): 53-59. 60. Havis, Emmanuelle, and Delphine Duprez. 'EGR1 transcription factor is a multifaceted regulator of matrix production in tendons and other connective tissues.' International journal of molecular sciences 21.5 (2020): 1664. 61. Milbrandt, Jeffrey. 'A nerve growth factor-induced gene encodes a possible transcriptional regulatory factor.' Science 238.4828 (1987): 797-799. 62. Sukhatme, V. P., et al. 'A novel early growth response gene rapidly induced by fibroblast, epithelial cell and lymphocyte mitogens.' Oncogene research 1.4 (1987): 343-355. 63. Sukhatme, Vikas P., et al. 'A zinc finger-encoding gene coregulated with c-fos during growth and differentiation, and after cellular depolarization.' Cell 53.1 (1988): 37-43. 64. Lim, Robert W., B. C. Varnum, and H. R. Herschman. 'Cloning of tetradecanoyl phorbol ester-induced'primary response'sequences and their expression in density-arrested Swiss 3T3 cells and a TPA non-proliferative variant.' Oncogene 1.3 (1987): 263-270. 65. Christy, Barbara A., Lester F. Lau, and Daniel Nathans. 'A gene activated in mouse 3T3 cells by serum growth factors encodes a protein with' zinc finger' sequences.' Proceedings of the National Academy of Sciences 85.21 (1988): 7857-7861. 66. Lemaire, Patrick, et al. 'Two mouse genes encoding potential transcription factors with identical DNA-binding domains are activated by growth factors in cultured cells.' Proceedings of the National Academy of Sciences 85.13 (1988): 4691-4695. 67. Havis, Emmanuelle, and Delphine Duprez. 'EGR1 transcription factor is a multifaceted regulator of matrix production in tendons and other connective tissues.' International journal of molecular sciences 21.5 (2020): 1664. 68. Gitenay, Delphine, and Véronique T. Baron. 'Is EGR1 a potential target for prostate cancer therapy?.' Future oncology 5.7 (2009): 993-1003. 69. Magee, Nancy, and Yuxia Zhang. 'Role of early growth response 1 in liver metabolism and liver cancer.' Hepatoma research 3 (2017): 268. 70. Eid, Manal A., et al. 'Expression of early growth response genes in human prostate cancer.' Cancer research 58.11 (1998): 2461-2468. 71. Park, Seon Young, et al. 'Expression of early growth response gene 1 in precancerous lesions of gastric cancer.' Oncology letters 12.4 (2016): 2710-2715. 72. Adamson, Eileen D., and Dan Mercola. 'Egr1 transcription factor: multiple roles in prostate tumor cell growth and survival.' Tumor biology 23.2 (2002): 93-102. 73. Abdulkadir, Sarki A., et al. 'Impaired prostate tumorigenesis in Egr1-deficient mice.' Nature medicine 7.1 (2001): 101-107. 74. Scharnhorst, Volkher, et al. 'EGR-1 enhances tumor growth and modulates the effect of the Wilms' tumor 1 gene products on tumorigenicity.' Oncogene 19.6 (2000): 791-800. 75. Huang, Ruo-Pan, et al. 'Egr-1 negatively regulates human tumor cell growth via the DNA-binding domain.' Cancer research 55.21 (1995): 5054-5062. 76. Maifrede, Silvia, et al. 'Loss of Egr1, a human del5q gene, accelerates BCR-ABL driven chronic myelogenous leukemia.' Oncotarget 8.41 (2017): 69281. 77. Mohamad, Trefa, et al. 'EGR1 interacts with TBX2 and functions as a tumor suppressor in rhabdomyosarcoma.' Oncotarget 9.26 (2018): 18084. 78. Krones-Herzig, Anja, et al. 'Early growth response 1 acts as a tumor suppressor in vivo and in vitro via regulation of p53.' Cancer research 65.12 (2005): 5133-5143. 79. Das, Anindita, et al. 'Ionizing radiation down-regulates p53 protein in primary Egr-1−/− mouse embryonic fibroblast cells causing enhanced resistance to apoptosis.' Journal of Biological Chemistry 276.5 (2001): 3279-3286. 80. Huang, Ruo‐Pan, et al. 'Decreased Egr‐1 expression in human, mouse and rat mammary cells and tissues correlates with tumor formation.' International journal of cancer 72.1 (1997): 102-109. 81. Wei, Lu-Lu, et al. 'Egr-1 suppresses breast cancer cells proliferation by arresting cell cycle progression via down-regulating CyclinDs.' International journal of clinical and experimental pathology 10.10 (2017): 10212. 82. Guan, Xiaowen, et al. 'EZH2 overexpression dampens tumor-suppressive signals via an EGR1 silencer to drive breast tumorigenesis.' Oncogene 39.48 (2020): 7127-7141. 83. Yang, Ming, et al. 'Sulforaphene inhibits triple negative breast cancer through activating tumor suppressor Egr1.' Breast cancer research and treatment 158.2 (2016): 277-286. 84. Crawford, N. T., et al. 'TBX2 interacts with heterochromatin protein 1 to recruit a novel repression complex to EGR1-targeted promoters to drive the proliferation of breast cancer cells.' Oncogene 38.31 (2019): 5971-5986. 85. Redmond, K. L., et al. 'T-box 2 represses NDRG1 through an EGR1-dependent mechanism to drive the proliferation of breast cancer cells.' Oncogene 29.22 (2010): 3252-3262. 86. Tarcic, Gabi, et al. 'EGR1 and the ERK‐ERF axis drive mammary cell migration in response to EGF.' The FASEB Journal 26.4 (2012): 1582-1592. 87. Tang, Tingting, et al. 'Protease Nexin I is a feedback regulator of EGF/PKC/MAPK/EGR1 signaling in breast cancer cells metastasis and stemness.' Cell death disease 10.9 (2019): 1-17. 88. Shajahan-Haq, Ayesha N., et al. 'EGR1 regulates cellular metabolism and survival in endocrine resistant breast cancer.' Oncotarget 8.57 (2017): 96865. 89. Cabodi, Sara, et al. 'Convergence of integrins and EGF receptor signaling via PI3K/Akt/FoxO pathway in early gene Egr‐1 expression.' Journal of cellular physiology 218.2 (2009): 294-303. 90. Mayer, Sabine I., et al. 'Epidermal-growth-factor-induced proliferation of astrocytes requires Egr transcription factors.' Journal of cell science 122.18 (2009): 3340-3350. 91. Cheng, J. C., H. M. Chang, and P. C. K. Leung. 'Egr-1 mediates epidermal growth factor-induced downregulation of E-cadherin expression via Slug in human ovarian cancer cells.' Oncogene 32.8 (2013): 1041-1049. 92. Lim, Cheh Peng, Neeraj Jain, and Xinmin Cao. 'Stress-induced immediate-early gene, egr-1, involves activation of p38/JNK1.' Oncogene 16.22 (1998): 2915-2926. 93. Shan, Jixiu, et al. 'A mitogen-activated protein kinase/extracellular signal-regulated kinase kinase (MEK)-dependent transcriptional program controls activation of the early growth response 1 (EGR1) gene during amino acid limitation.' Journal of Biological Chemistry 289.35 (2014): 24665-24679. 94. Shan, Jixiu, Elizabeth Dudenhausen, and Michael S. Kilberg. 'Induction of early growth response gene 1 (EGR1) by endoplasmic reticulum stress is mediated by the extracellular regulated kinase (ERK) arm of the MAPK pathways.' Biochimica et Biophysica Acta (BBA)-Molecular Cell Research 1866.3 (2019): 371-381. 95. Park, Seon Young, et al. 'Expression of early growth response gene 1 in precancerous lesions of gastric cancer.' Oncology letters 12.4 (2016): 2710-2715. 96. Dhillon, Amardeep Singh, et al. 'MAP kinase signalling pathways in cancer.' Oncogene 26.22 (2007): 3279-3290. 97. Almairac, Fabien, et al. 'ERK-mediated loss of miR-199a-3p and induction of EGR1 act as a “toggle switch” of GBM cell dedifferentiation into NANOG-and OCT4-positive cells.' Cancer research 80.16 (2020): 3236-3250. 98. Yeo, Hyunjin, et al. 'Transcription factor EGR-1 transactivates the MMP1 gene promoter in response to TNFα in HaCaT keratinocytes.' BMB reports 53.6 (2020): 323. 99. Kim, JuHwan, et al. 'WNT11 is a direct target of early growth response protein 1.' BMB reports 53.12 (2020): 628. 100. Burnatowska-Hledin, Maria A., et al. 'T47D breast cancer cell growth is inhibited by expression of VACM-1, a cul-5 gene.' Biochemical and biophysical research communications 319.3 (2004): 817-825. 101. Johnson, Alyssa E., et al. 'Estrogen-dependent growth and estrogen receptor (ER)-α concentration in T47D breast cancer cells are inhibited by VACM-1, a cul 5 gene.' Molecular and cellular biochemistry 301.1 (2007): 13-20. 102. Thiel, Gerald, and Giuseppe Cibelli. 'Regulation of life and death by the zinc finger transcription factor Egr‐1.' Journal of cellular physiology 193.3 (2002): 287-292. 103. Park, Seon Young, et al. 'Expression of early growth response gene 1 in precancerous lesions of gastric cancer.' Oncology letters 12.4 (2016): 2710-2715. 104. Liao, Yunjun, et al. 'Delayed hepatocellular mitotic progression and impaired liver regeneration in early growth response-1-deficient mice.' Journal of Biological Chemistry 279.41 (2004): 43107-43116. 105. Lee, Stephen L., et al. 'Growth and differentiation proceeds normally in cells deficient in the immediate early gene NGFI-A.' Journal of Biological Chemistry 270.17 (1995): 9971-9977. 106. O'Donovan, Kevin J., et al. 'The EGR family of transcription-regulatory factors: progress at the interface of molecular and systems neuroscience.' Trends in neurosciences 22.4 (1999): 167-173. 107. Steller, Hermann. 'Mechanisms and genes of cellular suicide.' Science 267.5203 (1995): 1445-1449. 108. Williams, Gwyn T. 'Programmed cell death: apoptosis and oncogenesis.' Cell (Cambridge) 65.7 (1991): 1097-1098. 109. Ahmed, Mansoor M., et al. 'EGR-1 induction is required for maximal radiosensitivity in A375-C6 melanoma cells.' Journal of Biological Chemistry 271.46 (1996): 29231-29237. 110. Nair, Prakash, et al. 'Early growth response-1-dependent apoptosis is mediated by p53.' Journal of biological chemistry 272.32 (1997): 20131-20138. 111. Yu, J., et al. 'A network of p73, p53 and Egr1 is required for efficient apoptosis in tumor cells.' Cell Death Differentiation 14.3 (2007): 436-446. 112. Ahmed, Mansoor M., et al. 'Ionizing radiation-inducible apoptosis in the absence of p53 linked to transcription factor EGR-1.' Journal of Biological Chemistry 272.52 (1997): 33056-33061. 113. Virolle, Thierry, et al. 'The Egr-1 transcription factor directly activates PTEN during irradiation-induced signalling.' Nature cell biology 3.12 (2001): 1124-1128. 114. Moorehead, Roger A., et al. 'Insulin-like growth factor-II regulates PTEN expression in the mammary gland.' Journal of biological chemistry 278.50 (2003): 50422-50427. 115. Thyss, Raphael, et al. 'NF‐κB/Egr‐1/Gadd45 are sequentially activated upon UVB irradiation to mediate epidermal cell death.' The EMBO journal 24.1 (2005): 128-137. 116. Huang, Ruo-Pan, et al. 'Egr-1 inhibits apoptosis during the UV response: correlation of cell survival with Egr-1 phosphorylation.' Cell Death Differentiation 5.1 (1998): 96-106. 117. DeSantis, Carol E., et al. 'Breast cancer statistics, 2017, racial disparity in mortality by state.' CA: a cancer journal for clinicians 67.6 (2017): 439-448. 118. Gupta, Gaorav P., and Joan Massagué. 'Cancer metastasis: building a framework.' Cell 127.4 (2006): 679-695. 119. Brabletz, Thomas, et al. 'EMT in cancer.' Nature Reviews Cancer 18.2 (2018): 128-134. 120. Kuo, Po‐Lin, et al. 'CXCL5/ENA78 increased cell migration and epithelial‐to‐mesenchymal transition of hormone‐independent prostate cancer by early growth response‐1/snail signaling pathway.' Journal of cellular physiology 226.5 (2011): 1224-1231. 121. Grotegut, Stefan, et al. 'Hepatocyte growth factor induces cell scattering through MAPK/Egr‐1‐mediated upregulation of Snail.' The EMBO journal 25.15 (2006): 3534-3545. 122. Ozen, Evin, et al. 'Heparin inhibits Hepatocyte Growth Factor induced motility and invasion of hepatocellular carcinoma cells through early growth response protein 1.' PloS one 7.8 (2012): e42717. 123. Wu, Wen-Sheng, et al. 'Snail collaborates with EGR-1 and SP-1 to directly activate transcription of MMP 9 and ZEB1.' Scientific reports 7.1 (2017): 1-13. 124. Sun, Ming, et al. 'The pseudogene DUXAP8 promotes non-small-cell lung cancer cell proliferation and invasion by epigenetically silencing EGR1 and RHOB.' Molecular Therapy 25.3 (2017): 739-751. 125. Kim, Jinkyung, et al. 'EGR1-dependent PTEN upregulation by 2-benzoyloxycinnamaldehyde attenuates cell invasion and EMT in colon cancer.' Cancer letters 349.1 (2014): 35-44. 126. Wong, Ka Ming, Jiaxing Song, and Yung H. Wong. 'CTCF and EGR1 suppress breast cancer cell migration through transcriptional control of Nm23-H1.' Scientific reports 11.1 (2021): 1-18. 127. Bléher, Marianne, et al. 'Egr1 loss-of-function promotes beige adipocyte differentiation and activation specifically in inguinal subcutaneous white adipose tissue.' Scientific reports 10.1 (2020): 1-15. 128. Milet, Cécile, et al. 'Egr1 deficiency induces browning of inguinal subcutaneous white adipose tissue in mice.' Scientific reports 7.1 (2017): 1-14. 129. Yu, Xiao, et al. 'Egr‐1 decreases adipocyte insulin sensitivity by tilting PI3K/Akt and MAPK signal balance in mice.' The EMBO journal 30.18 (2011): 3754-3765. 130. Shen, Ning, et al. 'An early response transcription factor, Egr-1, enhances insulin resistance in type 2 diabetes with chronic hyperinsulinism.' Journal of Biological Chemistry 286.16 (2011): 14508-14515. 131. Zhang, Jifeng, et al. 'Dietary obesity-induced Egr-1 in adipocytes facilitates energy storage via suppression of FOXC2.' Scientific reports 3.1 (2013): 1-10. 132. Gokey, Nolan G., et al. 'Early growth response 1 (Egr1) regulates cholesterol biosynthetic gene expression.' Journal of Biological Chemistry 286.34 (2011): 29501-29510. 133. Kim, JuHwan, et al. 'Leptin is a direct transcriptional target of EGR1 in human breast cancer cells.' Molecular biology reports 46.1 (2019): 317-324. 134. Nemani, Neeharika, et al. 'Mitochondrial pyruvate and fatty acid flux modulate MICU1-dependent control of MCU activity.' Science signaling 13.628 (2020). 135. Hanahan, Douglas, and Lisa M. Coussens. 'Accessories to the crime: functions of cells recruited to the tumor microenvironment.' Cancer cell 21.3 (2012): 309-322. 136. Petersen, Ole William, et al. 'Interaction with basement membrane serves to rapidly distinguish growth and differentiation pattern of normal and malignant human breast epithelial cells.' Proceedings of the National Academy of Sciences 89.19 (1992): 9064-9068. 137. Wang, Fei, et al. 'Reciprocal interactions between β1-integrin and epidermal growth factor receptor in three-dimensional basement membrane breast cultures: a different perspective in epithelial biology.' Proceedings of the National Academy of Sciences 95.25 (1998): 14821-14826. 138. Weaver, Valerie M., et al. 'Reversion of the malignant phenotype of human breast cells in three-dimensional culture and in vivo by integrin blocking antibodies.' The Journal of cell biology 137.1 (1997): 231-245. 139. Khaitan, Divya, et al. 'Differential mechanisms of radiosensitization by 2-deoxy-D-glucose in the monolayers and multicellular spheroids of a human glioma cell line.' Cancer biology therapy 5.9 (2006): 1142-1151. 140. Liao, Jianqun, et al. 'Ovarian cancer spheroid cells with stem cell-like properties contribute to tumor generation, metastasis and chemotherapy resistance through hypoxia-resistant metabolism.' PloS one 9.1 (2014): e84941. 141. Birgersdotter, Anna, Rickard Sandberg, and Ingemar Ernberg. 'Gene expression perturbation in vitro—a growing case for three-dimensional (3D) culture systems.' Seminars in cancer biology. Vol. 15. No. 5. Academic Press, 2005. 142. Kenny, Paraic A., et al. 'The morphologies of breast cancer cell lines in three-dimensional assays correlate with their profiles of gene expression.' Molecular oncology 1.1 (2007): 84-96. 143. Creighton, Chad, et al. 'Profiling of pathway-specific changes in gene expression following growth of human cancer cell lines transplanted into mice.' Genome biology 4.7 (2003): 1-12. 144. Edmondson, Rasheena, et al. 'Three-dimensional cell culture systems and their applications in drug discovery and cell-based biosensors.' Assay and drug development technologies 12.4 (2014): 207-218. 145. Hirschhaeuser, Franziska, et al. 'Multicellular tumor spheroids: an underestimated tool is catching up again.' Journal of biotechnology 148.1 (2010): 3-15. 146. Bell, H. S., et al. 'The development of necrosis and apoptosis in glioma: experimental findings using spheroid culture systems.' Neuropathology and applied neurobiology 27.4 (2001): 291-304. 147. Cui, X., Y. Hartanto, and H. Zhang. 'Advances in multicellular spheroids formation.' Journal of the Royal Society Interface 14.127 (2017): 20160877. 148. Zanoni, Michele, et al. '3D tumor spheroid models for in vitro therapeutic screening: a systematic approach to enhance the biological relevance of data obtained.' Scientific reports 6.1 (2016): 1-11. 149. Li, Qun, et al. '3D models of epithelial-mesenchymal transition in breast cancer metastasis: high-throughput screening assay development, validation, and pilot screen.' Journal of biomolecular screening 16.2 (2011): 141-154. 150. Froehlich, Karolin, et al. 'Generation of multicellular breast cancer tumor spheroids: comparison of different protocols.' Journal of mammary gland biology and neoplasia 21.3 (2016): 89-98. 151. Cheng, Chun-Ting, et al. 'Metabolic stress-induced phosphorylation of KAP1 Ser473 blocks mitochondrial fusion in breast cancer cells.' Cancer research 76.17 (2016): 5006-5018. 152. Moloney, Jennifer N., and Thomas G. Cotter. 'ROS signalling in the biology of cancer.' Seminars in cell developmental biology. Vol. 80. Academic Press, 2018. 153. Benton, Gabriel, et al. 'Matrigel™: from discovery and ECM mimicry to assays and models for cancer research.' Advanced drug delivery reviews 79 (f2014): 3-18. 154. Costa, Elisabete C., et al. 'Optimization of liquid overlay technique to formulate heterogenic 3D co‐cultures models.' Biotechnology and bioengineering 111.8 (2014): 1672-1685. 155. Su, Tianhong, et al. 'ΗΙF1α, EGR1 and SP1 co-regulate the erythropoietin receptor expression under hypoxia: an essential role in the growth of non-small cell lung cancer cells.' Cell Communication and Signaling 17.1 (2019): 1-12. 156. Wiederschain, Dmitri, et al. 'Single-vector inducible lentiviral RNAi system for oncology target validation.' Cell cycle 8.3 (2009): 498-504. 157. Pavlova, Natalya N., and Craig B. Thompson. 'The emerging hallmarks of cancer metabolism.' Cell metabolism 23.1 (2016): 27-47. 158. Kaspar, Sophie, et al. 'Adaptation to mitochondrial stress requires CHOP-directed tuning of ISR.' Science Advances 7.22 (2021): eabf0971. 159. Rutkowski, D. Thomas, et al. 'Adaptation to ER stress is mediated by differential stabilities of pro-survival and pro-apoptotic mRNAs and proteins.' PLoS Biol 4.11 (2006): e374. 160. B’chir, Wafa, et al. 'The eIF2α/ATF4 pathway is essential for stress-induced autophagy gene expression.' Nucleic acids research 41.16 (2013): 7683-7699. 161. Guan, Bo-Jhih, et al. 'Translational control during endoplasmic reticulum stress beyond phosphorylation of the translation initiation factor eIF2α.' Journal of Biological Chemistry 289.18 (2014): 12593-12611. 162. Krokowski, Dawid, et al. 'A self-defeating anabolic program leads to β-cell apoptosis in endoplasmic reticulum stress-induced diabetes via regulation of amino acid flux.' Journal of Biological Chemistry 288.24 (2013): 17202-17213. 163. Tabas, Ira, and David Ron. 'Integrating the mechanisms of apoptosis induced by endoplasmic reticulum stress.' Nature cell biology 13.3 (2011): 184-190. 164. Matsumoto, Hiroki, et al. 'Selection of autophagy or apoptosis in cells exposed to ER-stress depends on ATF4 expression pattern with or without CHOP expression.' Biology open 2.10 (2013): 1084-1090. 165. Huggins, Christopher J., et al. 'C/EBPγ is a critical regulator of cellular stress response networks through heterodimerization with ATF4.' Molecular and cellular biology 36.5 (2015): 693-713. 166. Guan, Bo-Jhih, et al. 'A unique ISR program determines cellular responses to chronic stress.' Molecular cell 68.5 (2017): 885-900. 167. Wortel, Inge MN, et al. 'Surviving stress: modulation of ATF4-mediated stress responses in normal and malignant cells.' Trends in Endocrinology Metabolism 28.11 (2017): 794-806. 168. Matheny, Cali, Mark L. Day, and Jeffrey Milbrandt. 'The nuclear localization signal of NGFI-A is located within the zinc finger DNA binding domain.' Journal of Biological Chemistry 269.11 (1994): 8176-8181. 169. Cao, Xinmin, et al. 'Protein phosphatase inhibitors induce the sustained expression of the Egr-1 gene and the hyperphosphorylation of its gene product.' Journal of Biological Chemistry 267.18 (1992): 12991-12997. 170. Manente, Arcangela Gabriella, et al. 'Coordinated sumoylation and ubiquitination modulate EGF induced EGR1 expression and stability.' PloS one 6.10 (2011): e25676. 171. Ma, Yibao, et al. 'Fatty acid oxidation: An emerging facet of metabolic transformation in cancer.' Cancer letters 435 (2018): 92-100. 172. Menendez, Javier A., and Ruth Lupu. 'Fatty acid synthase and the lipogenic phenotype in cancer pathogenesis.' Nature Reviews Cancer 7.10 (2007): 763-777. 173. Abramczyk, Halina, et al. 'The role of lipid droplets and adipocytes in cancer. Raman imaging of cell cultures: MCF10A, MCF-7, and MDA-MB-231 compared to adipocytes in cancerous human breast tissue.' Analyst 140.7 (2015): 2224-2235. 174. Jarc, Eva, et al. 'Lipid droplets induced by secreted phospholipase A2 and unsaturated fatty acids protect breast cancer cells from nutrient and lipotoxic stress.' Biochimica et Biophysica Acta (BBA)-Molecular and Cell Biology of Lipids 1863.3 (2018): 247-265. 175. Bensaad, Karim, et al. 'Fatty acid uptake and lipid storage induced by HIF-1α contribute to cell growth and survival after hypoxia-reoxygenation.' Cell reports 9.1 (2014): 349-365. 176. Huang, Ruo‐Pan, et al. 'Reciprocal modulation between Sp1 and Egr‐1.' Journal of cellular biochemistry 66.4 (1997): 489-499. 177. Tai, T. C……… | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/81028 | - |
| dc.description.abstract | 在固態實質腫瘤生長的過程中，癌細胞會大量消耗微環境中的氧氣及養份以滿足其快速生長的能量需求，尤其是距離腫瘤中心較近的癌細胞，其由血管提供的氧氣及養份也相對減少，導致腫瘤內產生代謝壓力。然而癌細胞會在遭受代謝壓力時改變代謝特性來適應不利的生存條件，甚至遷移至其他組織。在代謝壓力下癌細胞適應並生存的調控機制仍未被完整研究。 實驗室先前的研究分析了乳癌細胞MDA-MB-231在葡萄糖缺乏的情況下，其基因表達的變化，結果顯示轉錄因子EGR1顯著上調。作為一轉錄因子，EGR1已知會被多種壓力誘導並啟動下游基因的轉錄，研究證實其參與調節癌細胞的生長、遷移和侵襲，亦藉由凋亡調節細胞死亡，其在腫瘤生長的過程中扮演的角色仍未有定論。因此，我們試圖探討EGR1在代謝壓力下對於乳癌細胞適應性的調節作用。 本研究發現EGR1在葡萄糖、麩醯胺酸和精胺酸缺乏時會被誘導，且EGR1被誘導的情形在多種乳癌細胞株中皆可看到。我們亦建立三維細胞培養模型以模擬乳癌細胞遭受腫瘤內代謝壓力的情形，觀察到腫瘤球內產生代謝壓力時EGR1也有被誘導的現象，其表現量的增加和葡萄糖缺乏所造成的代謝壓力程度有關。 此外，EGR1被代謝壓力誘導的表現量上升是由ROS和p38路徑所調控，而EGR1的表現量上升顯著促進了細胞遷移，並有助於細胞在代謝壓力下生存，但並非透過抑制細胞內ROS的累積，且對於細胞凋亡僅有部分抑制。另一方面，小鼠實驗的結果顯示敲低EGR1顯著促進了小鼠體內乳癌腫瘤的生長，這可能是3D結構中各種養份及氧氣加成缺乏的結果。綜觀二維、三維細胞培養系統以及小鼠實驗的結果，我們推測EGR1在代謝壓力下對於乳癌細胞具有雙重作用，且其功能的轉換可能與代謝壓力的程度有關。透過探討EGR1的功能將有助於我們了解癌細胞如何感知並適應代謝壓力，進而區別對代謝壓力具有抗性的癌細胞群體，減少疾病的不良預後。 | zh_TW |
| dc.description.provenance | Made available in DSpace on 2022-11-24T03:26:53Z (GMT). No. of bitstreams: 1 U0001-3008202110464500.pdf: 4788277 bytes, checksum: f8fb4fb0eb45856f85588ebd3974504a (MD5) Previous issue date: 2021 | en |
| dc.description.tableofcontents | "致謝…………………………………………………………………………………i 中文摘要………………………………………………………………………………...ii English abstract…………………………………………………………………………iii 縮寫表……………………………………………………………………………...…....v 圖目錄…………………………………………………………….....ix 表目錄……………………………………………………………………………........xi 附圖目錄……………………………………………………………………………...xii 第一章 前言 1.1 乳癌…………………………………………………………………………...1 1.2 腫瘤內代謝壓力.……………………………………………………………...4 1.3 活性氧化物 (ROS) 平衡.…………………………………………………...6 1.4 早期生長反應家族 (Early Growth Response Family) ..………………...…....7 1.5 Early Growth Response 1 (EGR1)......…...………………………………….......8 1.5.1 EGR1的介紹………………………...……………………………….…8 1.5.2 EGR1與癌症………………………...…………………………………8 1.5.3 EGR1與乳癌………………………...…………………………………9 1.5.4 EGR1的誘導機制…………………...………………………………...9 1.5.5 EGR1與細胞增殖………………………...…………………………...10 1.5.6 EGR1與細胞凋亡………………………...……………………….…..11 1.5.7 EGR1與細胞轉移………………………...……………………….…..12 1.5.8 EGR1與細胞代謝………………………...……………………….…..13 1.6 3D培養模型…………...………........................……………….……..............13 1.6.1 3D培養模型的介紹…………...……………………….……...............14 1.6.2 3D腫瘤球的介紹……………...…………………….………...............14 第二章 研究目的………………………………………………………….………...16 第三章 研究方法 3.1 細胞培養與試劑……...…………………………………….......................17 3.2 慢病毒轉導和篩選…...…………………………………….......................17 3.3 RNAi基因敲低…………...………..……………………….........................18 3.4 RNA萃取…………...……………………………………............................18 3.5 反轉錄合成互補DNA…......……………………………............................19 3.6 及時定量聚合酶鏈鎖反應...........................................................19 3.7 蛋白質抽取及定量...……………………………………...........................19 3.8 西方墨點法...…………………………………….......................................20 3.9 質體建構及製備...……………………………...........................................20 3.9.1 pCMV Tag3A-hEGR1............................................20 3.9.2 pCDH-hEGR1.............................................22 3.9.3 Tet-shEGR1................................................23 3.10 免疫螢光染色........................................................24 3.11 細胞群落形成試驗.......................................................24 3.12 軟膠細胞群落形成試驗 (Soft agar assay) ................................24 3.13 酸性磷酸酶試驗 (Acid phosphatase test) ………………........................25 3.14 細胞總活性氧化物測定................................................25 3.15 細胞凋亡分析…………………………………........................................25 3.16 Trans-well細胞遷移試驗………………………………............................26 3.17 3D腫瘤球培養試驗……………………………........................................26 3.18 3D腫瘤球蛋白萃取………………………………....................................27 3.19 3D腫瘤球酸性磷酸酶試驗 (Acid phosphatase test) ........................27 3.20 3D腫瘤球冷凍切片.......................................................27 3.21 冷凍切片的螢光染色....................................................28 3.22 異種移植試驗...........................................................28 3.23 腫瘤組織RNA及蛋白質萃取...............................................28 3.24 基因集富集分析(GSEA)...............................................29 3.25 統計分析..............................................................29 第四章 結果 4.1 養份缺乏誘導EGR1表現....................................................30 4.2 葡萄糖缺乏誘導乳癌細胞中EGR1表現…................................................30 4.3 EGR1表現量在代謝壓力下被ROS, p38所調控.........................................31 4.4 建立EGR1克隆細胞系.............................................................31 4.5 EGR1在養份充足的情況下抑制乳癌細胞生長.........................................32 4.6 EGR1在代謝壓力下促進乳癌細胞存活...............................................32 4.7 EGR1在代謝壓力下不參與ROS的調控作用.............................................32 4.8 EGR1在代謝壓力下對乳癌細胞凋亡程度沒有明顯影響….....................33 4.9 EGR1在代謝壓力下促進MDA-MB-231細胞的遷移能力.........................33 4.10 腫瘤球培養模型的建立........................................................34 4.11 EGR1在3D腫瘤球中被誘導.........................................................35 4.12 EGR1抑制3D腫瘤球的細胞增殖....................................................35 4.13 EGR1在體內腫瘤生長後期抑制MDA-MB-231乳癌腫瘤發展...............36 4.14 建立Tet-on誘導敲低系統...................................................36 第五章 結論與討論………………………………………………...............................38 第六章 參考文獻.................................................................46圖.................................................................................67 表...........................................................................104 附圖........................................................................110 圖目錄 Figure 1 EGR1 expression is downregulated in breast cancer. …..................................67 Figure 2 Nutrient deprivation induces EGR1 expression in breast cancer cells. ……...68 Figure 3 EGR1 induction in breast cancer depends on glucose concentration. …....….70 Figure 4 Glucose deprivation induces EGR1 expression in various breast cancer cell lines. ……………………………………………………………………………………71 Figure 5 The induction of EGR1 upon glucose deprivation depends on ROS and p38 kinase activity. ……………………………………………………………………..…..72 Figure 6 Generation of the pCMV-Tag3A-hEGR1 clone. …………………………..…73 Figure 7 Generation of a stable EGR1-expressing cell line. …………………………..75 Figure 8 EGR1 represses the cell proliferation of breast cancer cells. …………..…….77 Figure 9 EGR1 overexpression promotes the viability of breast cancer cells under low glucose condition. ………………………………………………………………...……79 Figure 10 Knockdown of EGR1 represses the viability of breast cancer cells under low glucose condition. …………………………………………………………….………..80 Figure 11 Generation of EGR1 stable knockdown cell lines. ..….…….……..………..82 Figure 12 EGR1 does not affect ROS accumulation upon glucose deprivation. .…...…83 Figure 13 Knockdown of EGR1 only moderately affects apoptosis in breast cancer cells upon metabolic stress. ……………………………………………………………...…..85 Figure 14 EGR1 overexpression does not affect breast cancer cells apoptosis upon metabolic stress. ..………………….……………………………………………..…….87 Figure 15 Gene set enrichment analysis (GSEA) of breast cancer datasets reveals pathways correlated with EGR1 expression. ….…………….…………………......…..89 Figure 16 EGR1 promotes the migration of breast cancer cells under low glucose condition. ……….………………….……….…………………...…………….….…....91 Figure 17 VIM and SNAI1 promoters harbor EGR1 binding sites. …….....….…....…..92 Figure 18 3D spheroid formation assays of MCF-7 and MDA-MB-231 cells. ………..93 Figure 19 The induction of EGR1 expression in 3D spheroids. …………....……….....95 Figure 20 Immunofluorescence staining for EGR1 in MDA-MB-231 spheroids. .........96 Figure 21 Detection of MDA-MB-231 spheroid growth. ………...........…………..…..98 Figure 22 EGR1 represses the tumor growth in vivo. …..........….............…...........…...99 Figure 23 Generation of the Tet-shEGR1 clone. ………………………….……..…...101 Figure 24 The inducible knockdown efficiency of MDA-MB-231/Tet-shEGR1 cells. ..... ……………………….……..….....................……………………….……..…............102 Figure 25 Scheme illustrating the possible effects of EGR1 in breast cancer upon metabolic stress. ……………………………………………………..…….……..…...103 表目錄 Table 1 The top 20 genes induced upon glucose deprivation. ...................................104 Table 2 List of primers used for real-time qPCR. .....................................................105 Table 3 List of antibodies used for Western blots or immunofluorescence staining. 106 Table 4 List of primers used for building the EGR1 constructs. ...............................107 Table 5 List of primers used for constructs sequencing. ..........................................108 Table 6 List of sense and anti-sense oligonucleotide used for Tet-shEGR1 construct. ................................................................................109" | |
| dc.language.iso | zh-TW | |
| dc.subject | EGR1 | zh_TW |
| dc.subject | 乳癌 | zh_TW |
| dc.subject | 代謝壓力 | zh_TW |
| dc.subject | 養份缺乏 | zh_TW |
| dc.subject | EGR1 | en |
| dc.subject | breast cancer | en |
| dc.subject | metabolic stress | en |
| dc.subject | nutrient deprivation | en |
| dc.title | 探討 EGR1 在代謝壓力下對於乳癌細胞的作用 | zh_TW |
| dc.title | Investigating the Role of Early Growth Response 1 in Breast Cancer Cells under Intratumoral Metabolic Stress | en |
| dc.date.schoolyear | 109-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 林亮音(Hsin-Tsai Liu),楊雅倩(Chih-Yang Tseng),蘇剛毅 | |
| dc.subject.keyword | 乳癌,代謝壓力,養份缺乏,EGR1, | zh_TW |
| dc.subject.keyword | breast cancer,metabolic stress,nutrient deprivation,EGR1, | en |
| dc.relation.page | 112 | |
| dc.identifier.doi | 10.6342/NTU202102836 | |
| dc.rights.note | 同意授權(限校園內公開) | |
| dc.date.accepted | 2021-08-30 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 醫學檢驗暨生物技術學研究所 | zh_TW |
| 顯示於系所單位： | 醫學檢驗暨生物技術學系 | |
文件中的檔案：
| 檔案 | 大小 | 格式 | |
|---|---|---|---|
| U0001-3008202110464500.pdf 授權僅限NTU校內IP使用（校園外請利用VPN校外連線服務） | 4.68 MB | Adobe PDF |
系統中的文件，除了特別指名其著作權條款之外，均受到著作權保護，並且保留所有的權利。