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長非編碼RNA BANCR逆轉(zhuǎn)非小細(xì)胞肺癌細(xì)胞株順鉑耐藥的研究

發(fā)布時間:2018-01-29 05:34

  本文關(guān)鍵詞: 非小細(xì)胞肺癌 BANCR 順鉑耐藥性 出處:《南京醫(yī)科大學(xué)學(xué)報(自然科學(xué)版)》2017年02期  論文類型:期刊論文


【摘要】:目的:研究長非編碼RNA BANCR對人非小細(xì)胞肺癌耐順鉑細(xì)胞株A549/DDP耐藥性的影響及其可能的作用機制。方法:應(yīng)用實時熒光定量PCR法(q RT-PCR)檢測耐順鉑細(xì)胞株A549/DDP及其親本細(xì)胞株A549中BANCR的表達(dá)差異,發(fā)現(xiàn)BANCR在A549/DDP細(xì)胞中顯著低表達(dá)。在A549/DDP細(xì)胞中過表達(dá)BANCR,分別應(yīng)用MTT法、克隆形成實驗、流式細(xì)胞術(shù)檢測過表達(dá)后A549/DDP細(xì)胞對順鉑藥物敏感性,細(xì)胞增殖能力,聯(lián)合順鉑處理后細(xì)胞凋亡變化;Western blot檢測過表達(dá)BANCR后A549/DDP細(xì)胞p53的表達(dá)變化。結(jié)果:BANCR在A549/DDP細(xì)胞中的表達(dá)量顯著低于A549細(xì)胞(P0.05),在A549/DDP細(xì)胞中過表達(dá)BANCR可產(chǎn)生以下效應(yīng):相較于對照組,順鉑對A549/DDP/BANCR細(xì)胞的半數(shù)抑制濃度(half inhibition concentration,IC50)減低(P0.05),A549/DDP/BANCR細(xì)胞的增殖能力減弱,A549/DDP/BANCR經(jīng)過順鉑處理后細(xì)胞凋亡增多(P0.05)。Western blot結(jié)果顯示,與空白對照組比較,過表達(dá)BANCR的A549/DDP細(xì)胞p53表達(dá)水平明顯升高。結(jié)論:BANCR可能通過誘導(dǎo)細(xì)胞凋亡,抑制細(xì)胞增殖,上調(diào)p53蛋白表達(dá)而逆轉(zhuǎn)A549/DDP細(xì)胞對DDP的耐藥性。
[Abstract]:Objective: to study the effect of long non-coding RNA BANCR on drug resistance of cisplatin resistant human non-small cell lung cancer cell line A549 / DDP and its possible mechanism. Real-time fluorescence quantitative PCR method (. The expression of BANCR in cisplatin resistant A549 / DDP cell line and its parent A549 cell line was detected by Q RT-PCR. It was found that BANCR was significantly underexpressed in A549 / DDP cells, and BANCRs were overexpressed in A549 / DDP cells. MTT assay was used to clone the BANCRs in A549 / DDP cells. Flow cytometry was used to detect the sensitivity of A549% DDP cells to cisplatin, cell proliferation and apoptosis after treatment with cisplatin. The expression of p53 in A549 / DDP cells was detected by Western blot after BANCR expression. Results:. The expression of BANCR in A549 / DDP cells was significantly lower than that in A549 cells (. P0.05). Overexpression of BANCR in A549 / DDP cells had the following effects: compared with the control group. Half of the inhibitory concentration of cisplatin on A549 / DDP / BANCR cells was half inhibition concentration. IC50) reduced the proliferation ability of P0.05A549 / DDP / BANCR cells. Apoptosis of A549 / DDP / BANCR was increased after cisplatin treatment. The results of Western blot showed that the apoptosis of A549 / DDP / BANCR was higher than that of control group. The expression of p53 in A549 / DDP cells overexpression of BANCR was significantly increased. Conclusion: BANCR may inhibit cell proliferation by inducing cell apoptosis. The expression of p53 protein was upregulated and the drug resistance of A 549% DDP cells to DDP was reversed.
【作者單位】: 南京醫(yī)科大學(xué)第二附屬醫(yī)院腫瘤科;海門市人民醫(yī)院腫瘤科;
【基金】:國家自然科學(xué)基金(81272601,81472198) 江蘇省科技廳臨床醫(yī)學(xué)科技專項(BL2014096) 江蘇省醫(yī)學(xué)重點人才基金(RC2011080)
【分類號】:R734.2
【正文快照】: [Acta Univ Med Nanjing,2017,37(02):189-193]*通信作者(Corresponding author),E-mail:zhaoxiawang88@hotmail.com肺癌是世界范圍內(nèi)最常見惡性腫瘤之一,非小細(xì)胞肺癌(NSCLC)約占肺癌總數(shù)的80%以上[1],超過65%的患者為中晚期[2]。含鉑類方案為NSCLC化療重要的方案之一,而順鉑,

本文編號:1472672

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