本文選題：惡性腦膜瘤 + TMEM106B　； 參考：《南昌大學(xué)》2017年碩士論文

【摘要】：目的:觀察TMEM106B基因是否影響惡性腦膜瘤細(xì)胞的增殖和血管生成能力,并討論TMEM106B是否通過Her2信號(hào)通路發(fā)揮作用。方法:1、通過病毒感染沉默TMEM106B基因質(zhì)粒至惡性腦膜瘤IOMM-Lee和CH157細(xì)胞株中。實(shí)驗(yàn)分組:第一組:IOMM-Lee空白組(IOMM-Lee-blank);第二組:IOMM-Lee沉默陰性對(duì)照組(IOMM-Lee-NC-sh);第三組:IOMM-Lee沉默TMEM106B基因組(IOMM-Lee-TMEM106B-sh);第四組:CH157空白組(CH157-blank);第五組:CH157沉默陰性對(duì)照組(CH157-NC-sh);第六組CH157沉默TMEM106B基因組(CH157-TMEM106B-sh)。使用q-PCR、Western blot檢測(cè)各組細(xì)胞TMEM106B mRNA和蛋白表達(dá)水平。2、MTT、EdU法檢測(cè)各組細(xì)胞增殖情況;流式細(xì)胞術(shù)檢測(cè)各組細(xì)胞周期變化情況;小管形成實(shí)驗(yàn)檢測(cè)各組細(xì)胞血管生成情況。3、q-PCR和Western blot檢測(cè)各組細(xì)胞Her2、JUN和VEGF mRNA和蛋白表達(dá)水平。4、應(yīng)用Her2抑制劑Afatinib(BIBW2992)干擾惡性腦膜瘤細(xì)胞IOMM-Lee和CH157后,q-PCR和Western blot檢測(cè)Her2、JUN和VEGF mRNA和蛋白表達(dá)水平。結(jié)果:1、慢病毒轉(zhuǎn)染成功,TMEM106B在mRNA和蛋白水平達(dá)到分組要求。2、腦膜瘤細(xì)胞株IOMM-Lee和CH157沉默TMEM106B組細(xì)胞增殖和血管生成能力均減弱;TMEM106B基因通過影響細(xì)胞周期中的G0/G1-S的變化而起作用。3、沉默TMEM106B基因后,惡性腦膜瘤細(xì)胞IOMM-Lee和CH157的Her2和JUN基因m RNA和蛋白表達(dá)無明顯變化。4、干擾Her2基因后,惡性腦膜瘤細(xì)胞IOMM-Lee和CH157的TMEM106B和JUN基因m RNA和蛋白表達(dá)均減少。結(jié)論:1、TMEM106B可以促進(jìn)惡性腦膜瘤細(xì)胞株IOMM-Lee和CH157的增殖和血管生成;2、TMEM106B可能通過Her2信號(hào)通路影響惡性腦膜瘤細(xì)胞增殖和血管生成。
[Abstract]:Aim: to investigate whether TMEM106B gene affects the proliferation and angiogenesis of malignant meningioma cells and discuss whether TMEM106B plays a role through Her2 signaling pathway. Methods the TMEM106B gene plasmid was silenced by virus infection into IOMM-Lee and CH157 cell lines of malignant meningioma. The first group: IOMM-Lee-blank; the second group: IOMM-Lee-NC-sh; the third group: IOMM-Lee silencing TMEM106B (IOMM-Lee-TMEM106B-sh); the fourth group: CH157-blank; the fifth group: CH157-NC-sh; the sixth group CH157 silencing TMEM106B (CH157-TMEM106B-sh). The expression level of TMEM106B mRNA and protein was detected by q-PCRX Western blot. The proliferation of TMEM106B cells in each group was detected by TMEM106B mRNA and protein expression, and the cell cycle was detected by flow cytometry. The expression of Her2JUN and VEGF mRNA and protein in each group was detected by tubulogenesis assay and Western blot. Her2 inhibitor Afatinib (BIBW2992) was used to interfere with malignant meningioma cell line IOMM-Lee and CH157, and Western blot was used to detect Her2JUN and VEGFmRNA. And protein expression level. Results TMEM106B was successfully transfected with lentivirus to meet the requirement of grouping at mRNA and protein levels. The proliferation and angiogenesis ability of TMEM106B cells in meningioma cell lines IOMM-Lee and CH157 silenced by affecting the changes of G0 / G1-S in cell cycle was decreased. After silencing TMEM106B gene, The mRNA and protein expression of Her2 and Jun genes in malignant meningioma cell lines IOMM-Lee and CH157 showed no significant change. After interfering with Her2 gene, the mRNA and protein expressions of TMEM106B and Jun genes in IOMM-Lee and CH157 were decreased. Conclusion TMEM106B can promote the proliferation and angiogenesis of malignant meningioma cell lines IOMM-Lee and CH157. TMEM106B may affect the proliferation and angiogenesis of malignant meningioma cells through Her2 signaling pathway.
【學(xué)位授予單位】：南昌大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R739.45

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相關(guān)期刊論文 前2條

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本文編號(hào)：2082307