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http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/31013完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 王萬波 | |
| dc.contributor.author | Chun-Chiang Wen | en |
| dc.contributor.author | 溫俊強 | zh_TW |
| dc.date.accessioned | 2021-06-13T02:25:22Z | - |
| dc.date.available | 2012-02-02 | |
| dc.date.copyright | 2007-02-02 | |
| dc.date.issued | 2007 | |
| dc.date.submitted | 2007-01-29 | |
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/31013 | - |
| dc.description.abstract | HER2/neu屬於表皮生長因子接受器家族(epidermal growth factor receptor family；EGF receptor family)的一員。HER2/neu基因在許多人類癌症中時常有放大(amplification)或過度表現(overexpression)的現象，目前已知HER2/neu可以傳遞數個不同的信號路徑，這些路徑導致HER2/neu具有強大的致癌能力，因此，HER2/neu被認為是治療癌症的標的之一。
我們實驗室之前的研究證實了，SV40 T/t-common可以抑制HER2/neu啟動子的活性，並且可以抑制HER2/neu-overexpressing的卵巢癌細胞SK-OV-3中HER2/neu的表現量及其轉形活性。 在本論文中，我們進一步發現，T/t-common可以專一性的造成HER2/neu-overexpressing的癌細胞走向細胞凋亡，但是卻不會影響HER2/neu low-expressing的癌細胞或非轉形細胞。而T/t-common造成HER2/neu-overexpressing的癌細胞走向細胞凋亡，可能是透過抑制HER2/neu的表現，影響了細胞內MEK-ERK訊息傳遞，造成Bcl-2及Bcl-XL表現量下降，而導致細胞走向細胞凋亡。另外，我們也發現，T/t-common可以專一性的抑制HER2/neu-overexpressing的癌細胞在柔軟瓊脂產生聚落的能力，T/t-common亦具有抑制新生血管形成的潛力。以上結果顯示，T/t-common具有用於治療HER2/neu-overexpressing癌症的潛力。同時在本論文中，增加細胞中p300的表現量，仍然無法回復被T/t-common所抑制的HER2/neu啟動子的活性，因此，T/t-common並不是透過抑制p300而抑制了HER2/neu啟動子的活性。 | zh_TW |
| dc.description.abstract | HER2/neu gene (also known as erbB-2) is a proto-oncogene which belongs to the epidermal growth factor receptor family. It is overexpressed in many human cancers, including breast, lung, ovary, pancreas, gastric, and oral cancers. Overexpression of HER2/neu is associated with poor clinical outcome, including short survival time and short time to relapse. HER2/neu-overexpressing cancer cells usually have higher potential to proliferate, metastasize, induce angiogenesis, and resist chemotherapeutic agents. Inhibition of HER2/neu can lead to suppression of the tumorigenicity of HER2/neu-overexpressing cancer cells. Therefore HER2/neu gene is a suitable target for cancer treatment.
Previously we reported that simian virus 40 (SV40) T/t-common polypeptide, which contains the N-terminal common domain of SV40 large T and small t antigens, can repress HER2/neu expression and consequently suppress the tumorigenic potential of the HER2/neu-overexpressing ovarian carcinoma cells. Here we report that T/t-common could specifically induce apoptosis in HER2/neu-overexpressing human cancer cell lines but not in non-transformed cell lines and HER2/neu low-expressing human cancer cell lines. T/t-common’s ability to induce apoptosis in HER2/neu-overexpressing cancer cells was derived from its ability to inhibit HER2/neu, because re-expression of a large amount of HER2/neu could block apoptosis induced by T/t-common. T/t-common expression in HER2/neu-overexpressing SK-OV-3 cancer cells led to down-regulation of Bcl-2 and Bcl-XL, and overexpression of Bcl-2 could inhibit T/t-common’s ability to induce apoptosis in these cells. Therefore, T/t-common’s apoptosis-inducing activity is related to its ability to inhibit Bcl-2 expression in HER2/neu-overexpressing cancer cells. Consistent with T/t-common’s apoptosis-inducing activity, we found that T/t-common could specifically inhibit the soft-agarose colony-forming ability of the HER2/neu-overexpressing human cancer cell lines but not that of the HER2/neu low-expressing human cancer cell lines. Finally, we demonstrated that T/t-common could specifically sensitize HER2/neu-overexpressing human cancer cell lines, but not HER2/neu low-expressing human cancer cell lines, to chemotherapeutic agent etoposide. Together, these data suggest that T/t-common alone or in combination with chemotherapy may provide a new approach for treatment of cancers that overexpress HER2/neu. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-13T02:25:22Z (GMT). No. of bitstreams: 1 ntu-96-F90445111-1.pdf: 2603345 bytes, checksum: 402e9481371f26f5f6a01238519f7ff5 (MD5) Previous issue date: 2007 | en |
| dc.description.tableofcontents | 口試委員會審定書 ………………………………………………… i
中文摘要 …………………………………………………………… ii 英文摘要 …………………………………………………………… iii 縮寫表 ……………………………………………………………… v 緒論 ………………………………………………………………… 1 一、HER2/neu gene ……………………………………………… 1 二、HER2/neu和癌症的關係 …………………………………… 3 三、HER2/neu的訊息傳遞 ……………………………………… 4 四、針對HER2/neu-overexpressing癌症的治療………………… 5 五、猴病毒四十型（Simian virus 40）……………………… 10 六、SV40 大T抗原………………………………………………… 11 七、SV40小t 抗原………………………………………………… 12 八、SV40 LT and st common region (SV40 T/t-common) … 14 九、基因治療載體………………………………………………… 15 十、重組腺病毒載體……………………………………………… 18 研究目標…………………………………………………………… 20 材料與方法………………………………………………………… 21 結果 ……………………………………………………………… 47 一、SV40 T/t-common可導致HER2/neu-overexpressing的卵巢癌細胞SK-OV-3走向細胞凋亡 …………………………………………… 47 二、SV40 T/t-common導致HER2/neu-overexpressing癌細胞的細胞凋亡導因 於抑制HER2/neu的表現………………………………… 49 三、SV40 T/t-common導致HER2/neu-overexpressing癌細胞的細胞凋亡的分子機制……………………………………………………… 50 四、SV40 T/t-common可導致HER2/neu-overexpressing癌細胞的細胞凋亡，但不會造成nontransformed細胞及HER2/neu-low-expressing癌細胞的細胞凋亡……………………………………… 53 五、SV40 T/t-common可專一性的抑制HER2/neu-overexpressing癌細胞的轉 形能力 ………………………………………………… 54 六、T/t-common具有抑制新生血管生成的能力………………… 55 七、SV40 T/t-common抑制HER2/neu啟動子的機制探討………… 56 討論…………………………………………… …………………… 58 圖表 ………………………………………………………………… 64 附圖 ………………………………………………………………… 91 參考文獻 …………………………………………………………… 96 | |
| dc.language.iso | zh-TW | |
| dc.subject | tumor suppression | en |
| dc.subject | T/t-common | en |
| dc.subject | simian virus 40 (SV40) | en |
| dc.subject | HER2/neu | en |
| dc.subject | apoptosis | en |
| dc.title | 猴病毒四十型T/t-common蛋白質特異性地誘導HER2/neu大量表現的癌細胞走向細胞凋亡 | zh_TW |
| dc.title | SV40 T/t-Common Polypeptide Specifically Induces Apoptosis in Human Cancer Cells that Overexpress HER2/neu | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 95-1 | |
| dc.description.degree | 博士 | |
| dc.contributor.oralexamcommittee | 陳培哲,陳小梨,黃麗華,董馨蓮,鄧述諄 | |
| dc.subject.keyword | 人類表皮生長因子接受器,猴病毒四十型,大T小T共同區域,細胞凋亡,腫瘤抑制, | zh_TW |
| dc.subject.keyword | simian virus 40 (SV40),T/t-common,HER2/neu,apoptosis,tumor suppression, | en |
| dc.relation.page | 119 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2007-01-30 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 微生物學研究所 | zh_TW |
| 顯示於系所單位： | 微生物學科所 | |
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