本文關(guān)鍵詞： 宮頸癌 SA 上皮間質(zhì)轉(zhuǎn)化 PIK-Akt信號通路　出處：《中國生物工程雜志》2017年02期 　論文類型：期刊論文

【摘要】：目的:探討S100A6對人宮頸癌細(xì)胞系HeLa和SiHa增殖、遷移的影響及其機(jī)制。方法:首先采用定量聚合酶鏈反應(yīng)(quantitative polymerase chain reaction,qPCR)檢測宮頸癌細(xì)胞HeLa、SiHa和CaSki中S100A6 mRNA的基礎(chǔ)表達(dá),再分別采用重組腺病毒AdS100A6和AdsiS100A6干預(yù)HeLa和SiHa細(xì)胞,Western blot驗(yàn)證腺病毒感染是否成功;MTT法檢測細(xì)胞增殖能力,劃痕愈合試驗(yàn)檢測細(xì)胞遷移能力,Western blot檢測上皮間質(zhì)轉(zhuǎn)化(epithelial-mesenchymal transition,EMT)指標(biāo)E鈣粘蛋白(E-cadherin,E-cad)、N鈣粘蛋白(N-cadherin,N-cad)及p-Akt的蛋白水平,半定量反轉(zhuǎn)錄聚合酶鏈反應(yīng)(reverse transcription and polymerase chain reaction,RT-PCR)檢測PI3K-Akt信號通路下游靶基因Snail、Twist的表達(dá)。結(jié)果:與對照組相比,AdS100A6組的HeLa細(xì)胞3天時的OD_(492)值和劃痕愈合率均明顯升高,并伴隨E-cadherin降低和N-cadherin升高;而AdsiS100A6組的SiHa細(xì)胞5天時的OD_(492)值和3天時的劃痕愈合率明顯降低,并伴隨E-cadherin升高和N-cadherin降低;同時,在HeLa細(xì)胞中上調(diào)S100A6后p-Akt蛋白水平增加,該通路的下游靶基因Snail和Twist表達(dá)也明顯上調(diào)。結(jié)論:S100A6可以增強(qiáng)宮頸癌細(xì)胞的增殖和遷移能力,其機(jī)制可能涉及EMT和PI3K-Akt信號通路的激活。
[Abstract]:Objective: to investigate the effect of S100A6 on the proliferation and migration of human cervical cancer cell line HeLa and SiHa and its mechanism. Methods: the basic expression of S100A6 mRNA in cervical cancer cell line HeLa La SiHa and CaSki was detected by quantitative polymerase chain reactionqPCRs. Then the recombinant adenovirus AdS100A6 and AdsiS100A6 were used to test the proliferation of HeLa and SiHa cells by Western blot. The ability of cell migration was detected by scratch healing test and the levels of E-cadherin N-cadherin N-cadherin N-cadherin and p-Akt protein were detected by blot and E-cadherin E-cadherin N-cadherin N-cadherin N-cadherin and p-Akt protein levels in epithelium epithelial-mesenchymal transition. Semi-quantitative reverse transcription and polymerase chain reactionation polymerase chain reaction (RT-PCR) was used to detect the expression of the downstream target gene Snail-Twist in the PI3K-Akt signaling pathway. Results: compared with the control group, the HeLa cells in the AdS100A6 group were significantly higher in ODS-492) value and scratch healing rate than those in the control group. With the decrease of E-cadherin and the increase of N-cadherin, the number of SiHa cells in AdsiS100A6 group decreased significantly at 5 days and the rate of scratch healing at 3 days, and the E-cadherin increased and N-cadherin decreased, at the same time, the level of p-Akt protein increased after S100A6 was up-regulated in HeLa cells. The downstream target gene Snail and Twist expression were also up-regulated. Conclusion: S100A6 can enhance the proliferation and migration of cervical cancer cells, and its mechanism may be related to the activation of EMT and PI3K-Akt signaling pathway.
【作者單位】： 重慶醫(yī)科大學(xué)檢驗(yàn)醫(yī)學(xué)院臨床檢驗(yàn)診斷學(xué)教育部重點(diǎn)實(shí)驗(yàn)室;
【基金】：重慶市研究生科研創(chuàng)新資助項(xiàng)目(CYS15133)
【分類號】：R737.33

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