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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 林榮耀(Jung-Yaw Lin) | |
| dc.contributor.author | BO-SHAU CHEN | en |
| dc.contributor.author | 陳柏劭 | zh_TW |
| dc.date.accessioned | 2021-06-16T05:12:37Z | - |
| dc.date.available | 2019-10-09 | |
| dc.date.copyright | 2014-10-09 | |
| dc.date.issued | 2014 | |
| dc.date.submitted | 2014-08-18 | |
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/55998 | - |
| dc.description.abstract | Lung cancer is the leading cause of cancer deaths in Taiwan and worldwide, and the two major forms of lung cancer are non–small-cell lung cancer (NSCLC) (about 85% of all lung cancers) and small-cell lung cancer (about 15%). NSCLC is often diagnosed at an advanced stage and has a poor prognosis. It is frequently overexpressed and mutated (Ex: in-frame deletion △E746-A750 on exon 19, and L858R mutation on exon 20) in the Epidermal growth factor receptor (EGFR) during the development and progression of NSCLC. Recently, tyrosine kinase inhibitors (TKIs) have been used to treat selected NSCLC patients with EGFR mutations, but the long-term efficacy of such treatments is generally limited due to the development of resistance. Therefore, to develop novel therapeutic agents or strategies for the treatment of TKI-resistant tumors is urgently needed.
In this study, we set up a platform to screen extracts of CHMs on the inhibitory effects on the growth of H1975 cell line, which harbors EGFR T790M/L858R mutations and is resistant to TKIs, such as gefitinib. We found that the water extracts from NTU03 inhibited cell growth and proliferation of H1975 cells through Raf/Ras/Erk pathway. The extract also inhibited cell migration through FAK/Src signaling pathway and reduced RhoA activity, which led to inhibition of actin filament rearrangement and reduction of migration ability. In addition, extracts from NTU03 could attenuate Akt/Bcl2 signaling, promote Caspase-9/-3 and PARP cleavage, which then induced apoptosis. Besides, the level of VEGFA expression was reduced and the tube formation ability of human vascular endothelial cells was also suppressed. We further showed that NTU03 also had an inhibitory effect on tumor growth in vivo by a mouse xenograft model. By drug combination assay, we also found synergistic inhibitory effects of NTU03 combined with gefitinib on H1975 cell growth. Taken together, NTU03 may be a potential therapeutic agent for NSCLC treatment. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-16T05:12:37Z (GMT). No. of bitstreams: 1 ntu-103-R01442018-1.pdf: 2283084 bytes, checksum: 4046c38d4e0a54a8596e6fcebb0398be (MD5) Previous issue date: 2014 | en |
| dc.description.tableofcontents | Contents
摘要----------------------------------------------I Abstract---------------------------------------III Chapter 1. Introduction 2 1.Non-Small-Cell Lung Cancer (NSCLC)-------------3 2.NTU03------------------------------------------4 3.Epidermal growth factor receptor (EGFR)--------5 4.VEGF pathway-----------------------------------7 5.Rho-GTPase family------------------------------8 6.Research purpose of present investigation-----10 Chapter 2. Materials and Methods----------------11 1.Cell lines, Animals, and Reagents-------------12 2.Preparation of Chinese Herb Medicine (CHM)----13 3.Cell culture----------------------------------14 4.Cell viability assay--------------------------14 5.Cell migration/ invasion assay----------------15 6.Wound healing assay---------------------------15 7.Confocal microscopy---------------------------16 8.RNA extraction and reverse transcription------16 i. RNAs extraction------------------------------16 ii. Reverse transcription-----------------------17 9.Real time-quantitative PCR (Q-PCR)------------18 10.Western blot analysis------------------------19 i.Preparation of cell lysates:------------------19 ii.Quantification of protein concentration------19 iii.Preparation of sodium-dodecyl-sulfate-polyacrylamide gels (SDS-polyacrylamide gels)------------------20 iv.Protein sample preparation-------------------21 v.Electrophoresis-------------------------------22 vi.Wet and Semi-dry blotting--------------------22 vii.Immunoblotting------------------------------23 11.Nuclear and cytoplasmic fractionation--------24 12.GST-PBD/RBD pull down assay------------------25 i.Purification of GST-PBD (p21-binding domain, rac1 / cdc42 binding domain) and GST-RBD (Rho binding domain) from E.coli extracts----------------------------------------25 ii.Cdc42/Rac1 and RhoA activity assay-----------26 13.In vitro angiogenesis: endothelial cell tube formation Assay-------------------------------------------27 14.Measurement of F-Actin/G-Actin ratio---------27 15.Flow cytometry assay-------------------------28 16.Synergistic analysis of NTU03 with gefitinib-29 Chapter 3. Results------------------------------30 1.Cytotoxicity of NTU03 on three NSCLC cell lines (A549, H1975, and PC9)---------------------------------31 2.NTU03 showed inhibitory effects on migration/invasion of H1975 cells in a non-toxic manner---------------31 3.NTU03 disrupted the actin-filament rearrangement of H1975 cells by suppressing Rho-A activity via FAK/Src signaling. ------------------------------------------------32 4.NTU03 inhibited EGFR/Raf/ Erk signaling and induced G2/M arrest of H1975 cells.--------------------------33 5.NTU03 suppressed EGFR/ Akt signaling and induced apoptosis through Bcl2/Caspase-9,-3 pathways.-------------34 6.NTU03 suppressed STAT3/VEGFA signaling pathway.--35 7.NTU03 inhibited VEGF-induced migration and capillary structure formation of Human umbilical capillary endothelial cells (HUVECs)----------------------------------36 8.NTU03 decreased tumor growth in vivo.---------36 9.NTU03 had Synergistic effect with gefitinib on H1975 cells.------------------------------------------37 Chapter 4. Discussion---------------------------39 Chapter 5. Figures------------------------------45 Figure 1.Inhibitory effects of NTU03 on A549, H1975, and PC9 cell viability----------------------------------46 Figure 2.Inhibitory effects of NTU03 on A549, H1975, and PC9 cells proliferation-----------------------------47 Figure 3.NTU03 inhibited migration and invasion activity of A549, H1975, and PC9 cells.---------------------51 Figure 4.NTU03 disrupted the F-actin rearrangement via FAK/Src/RhoA signaling.-------------------------54 Figure 5.NTU03 inhibited EGFR/Raf/ Erk signaling and induced G2/M arrest of H1975 cells.---------------------56 Figure 6.NTU03 suppressed EGFR/ Akt signaling and induced apoptosis through Bcl2/Caspase-9,-3 pathways of H1975 cells. ------------------------------------------------58 Figure 7.Down-regulation of p-STAT3 and VEGF-A expression by the treatment of NTU03.-------------------------60 Figure 8.The NTU03 conditioned-medium inhibited the tube formation of HUVECs.----------------------------62 Figure 9.NTU03 inhibited tumor growth examined by mouse xenograft tumor models and IVIS image system.---64 Figure 10.NTU03 had Synergistic inhibitory effects with gefitinib on H1975 cells.-----------------------66 Figure 11.Mechanism of NTU03 inhibited H1975 cell migration, invasion, and angiogenesis.---------------------67 Chapter 6.Table---------------------------------68 Chapter 7.References----------------------------70 | |
| dc.language.iso | en | |
| dc.subject | 血管內皮生長因子-A | zh_TW |
| dc.subject | 血管新生 | zh_TW |
| dc.subject | 細胞爬行 | zh_TW |
| dc.subject | 中草藥 | zh_TW |
| dc.subject | 非小細胞肺癌 | zh_TW |
| dc.subject | Non-small-cell lung cancer (NSCLC) | en |
| dc.subject | Chinese Herbal Medicine (CHM) | en |
| dc.subject | Migration | en |
| dc.subject | Angiogenesis | en |
| dc.subject | VEGFA | en |
| dc.title | 中草藥: NTU03抗非小細胞肺癌之研究 | zh_TW |
| dc.title | Mechanisms of anti-Non-Small Cell Lung Cancer of Chinese
Herbal Medicine: NTU03 | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 102-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.coadvisor | 顏伯勳(Bo-Shiun Yan) | |
| dc.contributor.oralexamcommittee | 李明學(Ming-Shyue Lee),李德章(Te-Chang Lee) | |
| dc.subject.keyword | 非小細胞肺癌,中草藥,細胞爬行,血管新生,血管內皮生長因子-A, | zh_TW |
| dc.subject.keyword | Non-small-cell lung cancer (NSCLC),Chinese Herbal Medicine (CHM),Migration,Angiogenesis,VEGFA, | en |
| dc.relation.page | 75 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2014-08-19 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 生物化學暨分子生物學研究所 | zh_TW |
| 顯示於系所單位： | 生物化學暨分子生物學科研究所 | |
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