本文選題：卵巢癌 + p53抑癌基因��； 參考：《復(fù)旦大學(xué)》2014年碩士論文

【摘要】：目的：探索p53和Ras信號相互作用調(diào)節(jié)卵巢癌上皮細胞間質(zhì)轉(zhuǎn)化(EMT)、細胞衰老和細胞凋亡的機制。方法：在人卵巢漿液性乳頭狀囊腺癌細胞系SKOV3中導(dǎo)入能夠誘導(dǎo)表達的野生型p53以及H-Ras的四種不同突變體,建立細胞模型。在此基礎(chǔ)上,圍繞細胞衰老、細胞凋亡及EMT等,在細胞水平和動物水平上對p53和Ras在卵巢癌形成與發(fā)生過程中的相互作用進行了研究。結(jié)果：H-Ras(V12)能夠促進細胞凋亡和衰老的發(fā)生；H-Ras(E38)能夠較明顯促進凋亡的發(fā)生；H-Ras(S35)、H-Ras(C40)對細胞凋亡和衰老的誘導(dǎo)不明顯。誘導(dǎo)p53表達后,p53能夠促進各組腫瘤細胞凋亡和衰老,同時H-ras突變體蛋白的表達能夠?qū)筽53的抑癌作用。H-Ras (V12)、H-Ras (C40)具有較強的誘導(dǎo)EMT發(fā)生的能力。p53表達后,導(dǎo)入H-Ras (V12)、H-Ras (S35)、H-Ras (E38)的細胞的遷移能力和EMT的發(fā)生受到抑制；但對導(dǎo)入H-Ras(C40)突變體的細胞抑制作用不明顯。H-Ras (V12)、H-Ras (E38)導(dǎo)入細胞后體外克隆形成能力及體內(nèi)成瘤能力都減弱；H-Ras(S35)體外克隆形成能力及體內(nèi)成瘤能力影響不明顯,p53表達能夠在體內(nèi)和體外抑制其克隆形成及生長；H-Ras(C40)導(dǎo)入細胞后,細胞體外克隆形成能力增強,生長速度加快,在實驗動物體內(nèi)H-Ras(C40)能夠促進腫瘤的生長,且不能被p53抑制。結(jié)論：不同的H-ras突變體在卵巢癌的形成與發(fā)展過程中有不同的作用；p53的表達并不能完全抑制突變H-Ras在卵巢癌中的作用。目的探討樹舌靈芝提取物在實驗動物體內(nèi)對三陰乳腺癌的抑制作用。方法建立三陰乳腺癌荷瘤小鼠模型,觀察樹舌靈芝提取物對三陰乳腺癌的抑制作用作用;通過免疫組織化學(xué)染色,研究樹舌靈芝提取物抗腫瘤作用的機理。結(jié)果實體瘤模型中,樹舌靈芝組移植瘤重量和體積明顯低于對照組(P0.05),微血管密度值也低于對照組(P0.05);免疫組織化學(xué)染色結(jié)果顯示：樹舌靈芝組TSP-1表達升高;Cyclin D1表達降低。結(jié)論樹舌靈芝提取物在實驗動物體內(nèi),能通過抑制腫瘤組織中血管的生成并通過調(diào)節(jié)細胞周期來抑制腫瘤細胞的過度增殖,從而實現(xiàn)對三陰乳腺癌的抑制作用。
[Abstract]:Aim: to explore the mechanism of p53 and Ras signal interaction in regulating epithelial epithelial stromal transformation (EMT), cell senescence and apoptosis. Methods: four different mutants of wild-type p53 and H-Ras were introduced into human ovarian serous papillary cystadenocarcinoma cell line SKOV3. On this basis, the interaction of p53 and Ras in the formation and development of ovarian cancer was studied at cell level and animal level, focusing on cell senescence, apoptosis and EMT. Results: the cell apoptosis and senescence were promoted by the cell apoptosis induced by the cell apoptosis induced by H RasN S35 and H RasN C40 (P < 0 05), and the induction of cell apoptosis and senescence was not obvious (P < 0 05), and the induction of cell apoptosis and senescence was not obvious (P < 0 05). After p53 expression was induced, p53 could promote apoptosis and senescence of tumor cells in each group. Meanwhile, the expression of H-ras mutant protein could antagonize the tumor suppressor effect of p53. H-Ras V12H-Ras C40) had a strong ability to induce the expression of EMT. The ability of migration and the occurrence of EMT were inhibited in the cells transfected with H-Ras V12, H-Ras S35 and H-Ras (E38). But the cell inhibitory effect on the transfected H-Ras-C40) mutant was not obvious. H-Ras V12HRAS-E38) after the introduction of the cell line, the ability of colony formation in vitro and the ability of tumorigenesis in vivo were both weakened, and the ability of clone formation in vitro and tumorigenic ability in vivo were not significantly affected by the expression of p53. In vivo and in vitro, inhibition of the formation and growth of H- Rasn C40 was induced into the cells. The ability of cell clone formation was enhanced and the growth rate was accelerated in vitro. H-RasC40) could promote the growth of tumor and could not be inhibited by p53. Conclusion: different H-ras mutants play different roles in the formation and development of ovarian cancer. The expression of p53 can not completely inhibit the role of mutant H-Ras in ovarian cancer. Objective to investigate the inhibitory effect of Ganoderma lucidum extract on triple-negative breast cancer in experimental animals. Methods the tumor bearing mice model of Sanyin breast cancer was established to observe the inhibitory effect of Ganoderma lucidum extract on Sanyin breast cancer, and to study the anti-tumor mechanism of Ganoderma lucidum extract by immunohistochemical staining. Results in the solid tumor model, the weight and volume of transplanted tumor in Ganoderma lucidum group was significantly lower than that in control group (P 0.05), and the microvessel density was lower than that in control group (P 0.05). The results of immunohistochemical staining showed that the expression of Cyclin D1 in Ganoderma lucidum group was increased and Cyclin D1 expression was lower than that in Ganoderma lucidum group. Conclusion the Ganoderma lucidum extract can inhibit the proliferation of tumor cells by inhibiting the angiogenesis in tumor tissues and regulating the cell cycle so as to achieve the inhibitory effect on triple-negative breast cancer.
【學(xué)位授予單位】：復(fù)旦大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2014
【分類號】：R737.31

【共引文獻】

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本文編號：1788307