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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 張永祺 | zh_TW |
| dc.contributor.advisor | Yung-Chi Chang | en |
| dc.contributor.author | 翁子倓 | zh_TW |
| dc.contributor.author | Tzu-Tan Weng | en |
| dc.date.accessioned | 2025-09-22T16:09:08Z | - |
| dc.date.available | 2025-09-23 | - |
| dc.date.copyright | 2025-09-22 | - |
| dc.date.issued | 2025 | - |
| dc.date.submitted | 2025-08-05 | - |
| dc.identifier.citation | 1. Siegel, R.L., T.B. Kratzer, A.N. Giaquinto, H. Sung, and A. Jemal, Cancer statistics, 2025. CA Cancer J Clin, 2025. 75(1): p. 10-45.
2. Cancer Stat Facts: Colorectal Cancer. 2025; Available from: https://seer.cancer.gov/statfacts/html/colorect.html. 3. Simon, K., Colorectal cancer development and advances in screening. Clin Interv Aging, 2016. 11: p. 967-76. 4. Nguyen, H.T. and H.Q. Duong, The molecular characteristics of colorectal cancer: Implications for diagnosis and therapy. Oncol Lett, 2018. 16(1): p. 9-18. 5. Pinho, S.S. and C.A. Reis, Glycosylation in cancer: mechanisms and clinical implications. Nat Rev Cancer, 2015. 15(9): p. 540-55. 6. Hakomori, S. and R. Kannagi, Glycosphingolipids as tumor-associated and differentiation markers. J Natl Cancer Inst, 1983. 71(2): p. 231-51. 7. Marcos, N.T., E.P. Bennett, J. Gomes, A. Magalhaes, C. Gomes, et al., ST6GalNAc-I controls expression of sialyl-Tn antigen in gastrointestinal tissues. Front Biosci (Elite Ed), 2011. 3(4): p. 1443-55. 8. Julien, S., E. Adriaenssens, K. Ottenberg, A. Furlan, G. Courtand, et al., ST6GalNAc I expression in MDA-MB-231 breast cancer cells greatly modifies their O-glycosylation pattern and enhances their tumourigenicity. Glycobiology, 2006. 16(1): p. 54-64. 9. Amado, M., F. Carneiro, M. Seixas, H. Clausen, and M. Sobrinho-Simoes, Dimeric sialyl-Le(x) expression in gastric carcinoma correlates with venous invasion and poor outcome. Gastroenterology, 1998. 114(3): p. 462-70. 10. Nakamori, S., M. Kameyama, S. Imaoka, H. Furukawa, O. Ishikawa, et al., Increased expression of sialyl Lewisx antigen correlates with poor survival in patients with colorectal carcinoma: clinicopathological and immunohistochemical study. Cancer Res, 1993. 53(15): p. 3632-7. 11. Zhou, X., G. Yang, and F. Guan, Biological Functions and Analytical Strategies of Sialic Acids in Tumor. Cells, 2020. 9(2). 12. Wang, B., T. Zhang, S. Tang, C. Liu, C. Wang, et al., The physiological characteristics and applications of sialic acid. NPJ Sci Food, 2025. 9(1): p. 28. 13. Zhu, W., Y. Zhou, L. Guo, and S. Feng, Biological function of sialic acid and sialylation in human health and disease. Cell Death Discov, 2024. 10(1): p. 415. 14. Lenza, M.P., U. Atxabal, I. Oyenarte, J. Jimenez-Barbero, and J. Ereno-Orbea, Current Status on Therapeutic Molecules Targeting Siglec Receptors. Cells, 2020. 9(12). 15. Seales, E.C., G.A. Jurado, B.A. Brunson, J.K. Wakefield, A.R. Frost, et al., Hypersialylation of beta1 integrins, observed in colon adenocarcinoma, may contribute to cancer progression by up-regulating cell motility. Cancer Res, 2005. 65(11): p. 4645-52. 16. Smithson, M., S.A. Diffalha, R.K. Irwin, G. Williams, M.C. McLeod, et al., ST6GAL1 is associated with poor response to chemoradiation in rectal cancer. Neoplasia, 2024. 51: p. 100984. 17. Swindall, A.F. and S.L. Bellis, Sialylation of the Fas death receptor by ST6Gal-I provides protection against Fas-mediated apoptosis in colon carcinoma cells. J Biol Chem, 2011. 286(26): p. 22982-90. 18. Siddiqui, S.S., Non-canonical roles of Siglecs: Beyond sialic acid-binding and immune cell modulation. Molecular Aspects of Medicine, 2023. 90: p. 101145. 19. Angata, T. and A. Varki, Discovery, classification, evolution and diversity of Siglecs. Mol Aspects Med, 2023. 90: p. 101117. 20. Schwarz, F., C.S. Landig, S. Siddiqui, I. Secundino, J. Olson, et al., Paired Siglec receptors generate opposite inflammatory responses to a human-specific pathogen. Embo j, 2017. 36(6): p. 751-760. 21. Kuroki, K., A. Furukawa, and K. Maenaka, Molecular recognition of paired receptors in the immune system. Front Microbiol, 2012. 3: p. 429. 22. Angata, T., T. Hayakawa, M. Yamanaka, A. Varki, and M. Nakamura, Discovery of Siglec-14, a novel sialic acid receptor undergoing concerted evolution with Siglec-5 in primates. Faseb j, 2006. 20(12): p. 1964-73. 23. Yamanaka, M., Y. Kato, T. Angata, and H. Narimatsu, Deletion polymorphism of SIGLEC14 and its functional implications. Glycobiology, 2009. 19(8): p. 841-6. 24. Hayakawa, T., Z. Khedri, F. Schwarz, C. Landig, S.Y. Liang, et al., Coevolution of Siglec-11 and Siglec-16 via gene conversion in primates. BMC Evol Biol, 2017. 17(1): p. 228. 25. Wang, X., N. Mitra, P. Cruz, L. Deng, N.C.S. Program, et al., Evolution of siglec-11 and siglec-16 genes in hominins. Mol Biol Evol, 2012. 29(8): p. 2073-86. 26. Stanczak, M.A. and H. Laubli, Siglec receptors as new immune checkpoints in cancer. Mol Aspects Med, 2023. 90: p. 101112. 27. van de Wall, S., K.C.M. Santegoets, E.J.H. van Houtum, C. Bull, and G.J. Adema, Sialoglycans and Siglecs Can Shape the Tumor Immune Microenvironment. Trends Immunol, 2020. 41(4): p. 274-285. 28. Daly, J., S. Sarkar, A. Natoni, J.C. Stark, N.M. Riley, et al., Targeting hypersialylation in multiple myeloma represents a novel approach to enhance NK cell-mediated tumor responses. Blood Adv, 2022. 6(11): p. 3352-3366. 29. Jandus, C., K.F. Boligan, O. Chijioke, H. Liu, M. Dahlhaus, et al., Interactions between Siglec-7/9 receptors and ligands influence NK cell-dependent tumor immunosurveillance. J Clin Invest, 2014. 124(4): p. 1810-20. 30. Haas, Q., K.F. Boligan, C. Jandus, C. Schneider, C. Simillion, et al., Siglec-9 Regulates an Effector Memory CD8(+) T-cell Subset That Congregates in the Melanoma Tumor Microenvironment. Cancer Immunol Res, 2019. 7(5): p. 707-718. 31. Stanczak, M.A., S.S. Siddiqui, M.P. Trefny, D.S. Thommen, K.F. Boligan, et al., Self-associated molecular patterns mediate cancer immune evasion by engaging Siglecs on T cells. J Clin Invest, 2018. 128(11): p. 4912-4923. 32. Laubli, H., O.M. Pearce, F. Schwarz, S.S. Siddiqui, L. Deng, et al., Engagement of myelomonocytic Siglecs by tumor-associated ligands modulates the innate immune response to cancer. Proc Natl Acad Sci U S A, 2014. 111(39): p. 14211-6. 33. Wang, Q., X. Shao, Y. Zhang, M. Zhu, F.X.C. Wang, et al., Role of tumor microenvironment in cancer progression and therapeutic strategy. Cancer Med, 2023. 12(10): p. 11149-11165. 34. Chun, E., S. Lavoie, M. Michaud, C.A. Gallini, J. Kim, et al., CCL2 Promotes Colorectal Carcinogenesis by Enhancing Polymorphonuclear Myeloid-Derived Suppressor Cell Population and Function. Cell Rep, 2015. 12(2): p. 244-57. 35. Paauwe, M., M.J.A. Schoonderwoerd, R. Helderman, T.J. Harryvan, A. Groenewoud, et al., Endoglin Expression on Cancer-Associated Fibroblasts Regulates Invasion and Stimulates Colorectal Cancer Metastasis. Clin Cancer Res, 2018. 24(24): p. 6331-6344. 36. Pittet, M.J., O. Michielin, and D. Migliorini, Clinical relevance of tumour-associated macrophages. Nat Rev Clin Oncol, 2022. 19(6): p. 402-421. 37. Zhang, Q.W., L. Liu, C.Y. Gong, H.S. Shi, Y.H. Zeng, et al., Prognostic significance of tumor-associated macrophages in solid tumor: a meta-analysis of the literature. PLoS One, 2012. 7(12): p. e50946. 38. Wang, H., T. Tian, and J. Zhang, Tumor-Associated Macrophages (TAMs) in Colorectal Cancer (CRC): From Mechanism to Therapy and Prognosis. Int J Mol Sci, 2021. 22(16). 39. Pan, Y., Y. Yu, X. Wang, and T. Zhang, Tumor-Associated Macrophages in Tumor Immunity. Front Immunol, 2020. 11: p. 583084. 40. Chen, Y., Y. Song, W. Du, L. Gong, H. Chang, et al., Tumor-associated macrophages: an accomplice in solid tumor progression. J Biomed Sci, 2019. 26(1): p. 78. 41. Tamura, R., T. Tanaka, Y. Yamamoto, Y. Akasaki, and H. Sasaki, Dual role of macrophage in tumor immunity. Immunotherapy, 2018. 10(10): p. 899-909. 42. Steenbrugge, J., K. Breyne, K. Demeyere, O. De Wever, N.N. Sanders, et al., Anti-inflammatory signaling by mammary tumor cells mediates prometastatic macrophage polarization in an innovative intraductal mouse model for triple-negative breast cancer. J Exp Clin Cancer Res, 2018. 37(1): p. 191. 43. Song, W., R. Mazzieri, T. Yang, and G.C. Gobe, Translational Significance for Tumor Metastasis of Tumor-Associated Macrophages and Epithelial-Mesenchymal Transition. Front Immunol, 2017. 8: p. 1106. 44. Arlauckas, S.P., S.B. Garren, C.S. Garris, R.H. Kohler, J. Oh, et al., Arg1 expression defines immunosuppressive subsets of tumor-associated macrophages. Theranostics, 2018. 8(21): p. 5842-5854. 45. Rodriguez, P.C., D.G. Quiceno, J. Zabaleta, B. Ortiz, A.H. Zea, et al., Arginase I production in the tumor microenvironment by mature myeloid cells inhibits T-cell receptor expression and antigen-specific T-cell responses. Cancer Res, 2004. 64(16): p. 5839-49. 46. Luo, M., F. Zhao, H. Cheng, M. Su, and Y. Wang, Macrophage polarization: an important role in inflammatory diseases. Front Immunol, 2024. 15: p. 1352946. 47. Takamiya, R., K. Ohtsubo, S. Takamatsu, N. Taniguchi, and T. Angata, The interaction between Siglec-15 and tumor-associated sialyl-Tn antigen enhances TGF-beta secretion from monocytes/macrophages through the DAP12-Syk pathway. Glycobiology, 2013. 23(2): p. 178-87. 48. Beatson, R., V. Tajadura-Ortega, D. Achkova, G. Picco, T.D. Tsourouktsoglou, et al., The mucin MUC1 modulates the tumor immunological microenvironment through engagement of the lectin Siglec-9. Nat Immunol, 2016. 17(11): p. 1273-1281. 49. Barkal, A.A., R.E. Brewer, M. Markovic, M. Kowarsky, S.A. Barkal, et al., CD24 signalling through macrophage Siglec-10 is a target for cancer immunotherapy. Nature, 2019. 572(7769): p. 392-396. 50. Yin, J., Y. Lu, Y. Liu, Q. Shi, M. Shi, et al., SIGLEC11 promotes M2 macrophage polarization through AKT-mTOR signaling and facilitates the progression of gastric cancer. J Immunother Cancer, 2025. 13(1). 51. Ali, S.R., J.J. Fong, A.F. Carlin, T.D. Busch, R. Linden, et al., Siglec-5 and Siglec-14 are polymorphic paired receptors that modulate neutrophil and amnion signaling responses to group B Streptococcus. J Exp Med, 2014. 211(6): p. 1231-42. 52. Läubli, H. and A. Varki, Sialic acid-binding immunoglobulin-like lectins (Siglecs) detect self-associated molecular patterns to regulate immune responses. Cell Mol Life Sci, 2020. 77(4): p. 593-605. 53. Boutilier, A.J. and S.F. Elsawa, Macrophage Polarization States in the Tumor Microenvironment. Int J Mol Sci, 2021. 22(13). 54. Xie, Z., G. Zheng, L. Niu, K. Du, R. Li, et al., SPP1 (+) macrophages in colorectal cancer: Markers of malignancy and promising therapeutic targets. Genes Dis, 2025. 12(3): p. 101340. 55. Mocsai, A., J. Ruland, and V.L. Tybulewicz, The SYK tyrosine kinase: a crucial player in diverse biological functions. Nat Rev Immunol, 2010. 10(6): p. 387-402. 56. Uckun, F.M., S. Qazi, H. Ma, L. Tuel-Ahlgren, and Z. Ozer, STAT3 is a substrate of SYK tyrosine kinase in B-lineage leukemia/lymphoma cells exposed to oxidative stress. Proc Natl Acad Sci U S A, 2010. 107(7): p. 2902-7. 57. Shields, N.J., E.M. Peyroux, A.L. Ferguson, M. Steain, S. Neumann, et al., Late-stage MC38 tumours recapitulate features of human colorectal cancer - implications for appropriate timepoint selection in preclinical studies. Front Immunol, 2023. 14: p. 1152035. 58. DeNiro, G., K. Que, T. Fujimoto, S.M. Koo, B. Schneider, et al., OMIP-105: A 30-color full-spectrum flow cytometry panel to characterize the immune cell landscape in spleen and tumor within a syngeneic MC-38 murine colon carcinoma model. Cytometry A, 2024. 105(9): p. 659-665. 59. Zhu, S., M. Yi, Y. Wu, B. Dong, and K. Wu, Roles of tumor-associated macrophages in tumor progression: implications on therapeutic strategies. Exp Hematol Oncol, 2021. 10(1): p. 60. 60. Dzhalilova, D., N. Zolotova, N. Fokichev, and O. Makarova, Murine models of colorectal cancer: the azoxymethane (AOM)/dextran sulfate sodium (DSS) model of colitis-associated cancer. PeerJ, 2023. 11: p. e16159. 61. Kim, J.J., M.S. Shajib, M.M. Manocha, and W.I. Khan, Investigating intestinal inflammation in DSS-induced model of IBD. J Vis Exp, 2012(60). 62. Kiesler, P., I.J. Fuss, and W. Strober, Experimental Models of Inflammatory Bowel Diseases. Cell Mol Gastroenterol Hepatol, 2015. 1(2): p. 154-170. 63. Dhillon, A.S., S. Hagan, O. Rath, and W. Kolch, MAP kinase signalling pathways in cancer. Oncogene, 2007. 26(22): p. 3279-90. 64. Cheng, Y., Y. Zhu, W. Xu, J. Xu, M. Yang, et al., PKCalpha in colon cancer cells promotes M1 macrophage polarization via MKK3/6-P38 MAPK pathway. Mol Carcinog, 2018. 57(8): p. 1017-1029. 65. Ganguly, P., T. Macleod, C. Wong, M. Harland, and D. McGonagle, Revisiting p38 Mitogen-Activated Protein Kinases (MAPK) in Inflammatory Arthritis: A Narrative of the Emergence of MAPK-Activated Protein Kinase Inhibitors (MK2i). Pharmaceuticals (Basel), 2023. 16(9). 66. Fan, M.K., G.C. Zhang, W. Chen, L.L. Qi, M.F. Xie, et al., Siglec-15 Promotes Tumor Progression in Osteosarcoma via DUSP1/MAPK Pathway. Front Oncol, 2021. 11: p. 710689. 67. Maniaci, B., D. Friedman, S. Crotts, A. Zastrow, K. Martinez, et al., Siglec-E functions as a brake for intestinal inammation to protect fromcolitis-associated cancer. Journal of Immunology, 2024. 212(1). 68. Cuello, H.A., S. Sinha, A.L. Verhagen, N. Varki, A. Varki, et al., Human-specific elimination of epithelial Siglec-XII suppresses the risk of inflammation-driven colorectal cancers. JCI Insight, 2024. 9(16). | - |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/99961 | - |
| dc.description.abstract | 腫瘤細胞常具有過度唾液酸化的特徵，並可透過與腫瘤微環境中免疫細胞表面的唾液酸受體Siglec結合，幫助其逃脫免疫監視並促進腫瘤進展。已知巨噬細胞表面的Siglec-5與Siglec-14成對受體可辨識相同的唾液酸配體，但分別傳遞抑制型與活化型訊號。由於大腸癌細胞表面常大量表現唾液酸，本研究旨在探討此對訊號相反的受體是否以不同方式調控巨噬細胞極化。我們發現，於標準第二型細胞激素mIL-4或小鼠大腸癌細胞MC38細胞培養液(CM)刺激下，表現 Siglec-14的骨髓源性巨噬細胞(S14/BMDM)更趨向於M2或腫瘤相關巨噬細胞(TAM)的表型，並且相較WT/BMDM表現較高的SYK與ERK磷酸化，但p38的磷酸化表現較低；相對地，表現Siglec-5的BMDM (S5/BMDM)則無顯著極化影響，S5/BMDM中SYK、ERK及p38磷酸化程度則低於WT/BMDM。在MC38皮下腫瘤模型當中，我們觀察到SIGLEC14Myeloid TG小鼠腫瘤生長快速且體積較大，伴隨NK細胞浸潤減少與巨噬細胞浸潤增加；而SIGLEC5Myeloid TG小鼠之免疫細胞組成和腫瘤生長則與 WT 小鼠相似。在AOM/DSS誘導的大腸直腸癌模型中，SIGLEC14Myeloid TG小鼠大腸腫瘤體積顯著增加，並呈現黏膜內腺癌特徵及嚴重黏膜損傷；而SIGLEC5Myeloid TG小鼠的腫瘤大小則與WT小鼠無顯著差異。綜合上述，我們發現Siglec-14 可促進巨噬細胞極化為 M2/TAM 表型，進而推動腫瘤生長與免疫抑制環境的建立。惟其與唾液酸配體結合後如何調控巨噬細胞訊息傳導與腫瘤進程，尚待進一步研究釐清。 | zh_TW |
| dc.description.abstract | Tumor cells often overexpress sialic acids, which engage Siglecs (sialic acid–binding immunoglobulin-like lectins) on immune cells to evade immune surveillance and promote tumor progression within the tumor microenvironment. Among Siglecs, Siglec-5 and Siglec-14 are paired receptors expressed on macrophages that recognize the same sialylated ligands but transmit opposing signals: Siglec-5 delivers inhibitory signals, while Siglec-14 activates immune responses. Given that colorectal cancer (CRC) cells are known to express high levels of sialic acids, we investigated the role of Siglec-5 and Siglec-14 in macrophage polarization and tumor development in murine CRC models. We found that bone marrow–derived macrophages (BMDMs) expressing Siglec-14 (S14/BMDMs) showed enhanced M2 or tumor-associated macrophage (TAM) polarization when stimulated with IL-4 or conditioned medium from murine CRC MC38 cells (MC38 CM). Under these conditions, S14/BMDMs exhibited increased phosphorylation of SYK and ERK and reduced phosphorylation of p38 compared to wild-type BMDMs. In contrast, BMDMs expressing Siglec-5 (S5/BMDMs) did not display enhanced polarization, and phosphorylation of SYK, ERK, and p38 was lower than in wild-type controls. In the AOM/DSS-induced spontaneous CRC model, SIGLEC14Myeloid TG mice developed larger tumors with intramucosal adenocarcinoma features and severe mucosal damage. Tumor sizes were comparable between SIGLEC5Myeloid TG and wild-type mice. Similarly, in the MC38 subcutaneous tumor model, SIGLEC14Myeloid TG mice exhibited larger and faster-growing tumors, accompanied by reduced NK cell infiltration and increased macrophage infiltration. Tumor growth and immune cell composition was comparable between SIGLEC5Myeloid TG and wild-type mice. Together, our findings suggest that Siglec-14 promotes macrophage polarization toward the M2/TAM phenotype, enhancing tumor growth and immune suppression in CRC models. However, the precise mechanism by which Siglec-14 interacts with its ligands to modulate macrophage signaling and influence tumor progression remains to be elucidated. | en |
| dc.description.provenance | Submitted by admin ntu (admin@lib.ntu.edu.tw) on 2025-09-22T16:09:08Z No. of bitstreams: 0 | en |
| dc.description.provenance | Made available in DSpace on 2025-09-22T16:09:08Z (GMT). No. of bitstreams: 0 | en |
| dc.description.tableofcontents | 口試委員會審定書 i
致謝 ii 中文摘要 iii Abstract iv 目次 vi 壹、研究背景與動機 1 一、大腸直腸癌的發生以及與唾液酸的關係 1 1. 大腸直腸癌簡介 1 2. 醣基化(Glycosylation)在癌症中的角色 1 3. 唾液酸(sialic acid)與大腸直腸癌的關係 2 二、Sialic acid-binding immunoglobulin-like lectin (Siglec) 3 1. Siglec簡介 3 2. Siglec與腫瘤免疫之關係 5 三、腫瘤相關巨噬細胞 (Tumor-associated macrophage) 6 1. 腫瘤相關巨噬細胞在腫瘤微環境的功能 6 2. Siglec對巨噬細胞極化的影響 7 四、研究動機 8 貳、實驗材料與研究方法 10 一、實驗材料 10 1.細胞株(Cell lines) 10 2.抗體(Antibodies) 10 3.引子(Primers) 11 4.抗生素(Antibiotics) 12 5.小鼠來源 12 二、研究方法 12 1.取得癌細胞培養液(CM) 12 2.取得L929細胞培養液 12 3.培育帶有人類SIGLEC5與SIGLEC14基因轉殖小鼠 13 4.小鼠基因型分型(Genotyping) 13 5.取得骨髓源性巨噬細胞(BMDM) 13 6.巨噬細胞極化 14 7.定量反轉錄聚合酶連鎖反應(RT-qPCR) 14 8.西方墨點法(Western blot) 15 9.氧化偶氮甲烷合併葡聚醣硫酸鈉誘導的小鼠發炎性大腸直腸癌模型 15 10.免疫組織化學染色法 16 11.同源腫瘤移植模型 17 12.流式細胞儀分析(Flow cytometry analysis) 17 參、研究結果 19 一、Siglec-5與Siglec-14在SIGLEC5Myeloid TG和SIGLEC14Myeloid TG表現情形 19 二、Siglec-5與Siglec-14對mIL-4所誘導的M2巨噬細胞極化之影響 19 三、Siglec-5與Siglec-14對大腸癌細胞MC38 CM所誘導的腫瘤相關巨噬細胞極化之影響 20 四、Siglec-5與Siglec-14對SYK活化以及IL-4下游路徑的調控探討 21 五、Siglec-5與Siglec-14對MC38 CM刺激後下游路徑調控探討 23 六、Siglec-5與Siglec-14在小鼠皮下MC38腫瘤模型中對於腫瘤生長免疫細胞浸潤情形之影響 24 七、Siglec-5與Siglec-14在發炎性大腸直腸癌模型中對腫瘤生長之影響 25 肆、討論與未來方向 27 參考文獻 32 研究圖表 38 附錄 65 | - |
| dc.language.iso | zh_TW | - |
| dc.subject | Siglec-14 | zh_TW |
| dc.subject | Siglec-5 | zh_TW |
| dc.subject | 腫瘤相關巨噬細胞 | zh_TW |
| dc.subject | 巨噬細胞極化 | zh_TW |
| dc.subject | 腫瘤生長 | zh_TW |
| dc.subject | macrophage polarization | en |
| dc.subject | tumor-associated macrophages | en |
| dc.subject | tumor growth | en |
| dc.subject | Siglec-14 | en |
| dc.subject | Siglec-5 | en |
| dc.title | 探討成對受體 Siglec-5 與 Siglec-14 在 巨噬細胞極化與小鼠大腸直腸癌模型中的角色 | zh_TW |
| dc.title | Investigating the role of paired receptor Siglec-5 and Siglec-14 in macrophage polarization and murine colorectal tumor models | en |
| dc.type | Thesis | - |
| dc.date.schoolyear | 113-2 | - |
| dc.description.degree | 碩士 | - |
| dc.contributor.oralexamcommittee | 李明學;余佳慧 | zh_TW |
| dc.contributor.oralexamcommittee | Ming-Shyue Lee;Chia-Hui Yu | en |
| dc.subject.keyword | Siglec-5,Siglec-14,腫瘤生長,巨噬細胞極化,腫瘤相關巨噬細胞, | zh_TW |
| dc.subject.keyword | Siglec-5,Siglec-14,macrophage polarization,tumor-associated macrophages,tumor growth, | en |
| dc.relation.page | 65 | - |
| dc.identifier.doi | 10.6342/NTU202503947 | - |
| dc.rights.note | 未授權 | - |
| dc.date.accepted | 2025-08-05 | - |
| dc.contributor.author-college | 醫學院 | - |
| dc.contributor.author-dept | 微生物學研究所 | - |
| dc.date.embargo-lift | N/A | - |
| 顯示於系所單位： | 微生物學科所 | |
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| ntu-113-2.pdf 未授權公開取用 | 5.16 MB | Adobe PDF |
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