抑制自噬增強門冬酰胺酶對小細胞肺癌細胞H1688和H446的抗癌作用
發(fā)布時間:2018-05-27 17:22
本文選題:小細胞肺癌 + 門冬酰胺酶; 參考:《第三軍醫(yī)大學學報》2017年06期
【摘要】:目的研究門冬酰胺酶(asparaginase,AN)對小細胞肺癌H1688和H446細胞的抗癌作用,探討自噬在AN抗癌過程中的功能。方法采用MTT法及臺盼藍染色法檢測AN單獨或聯(lián)用自噬抑制劑氯喹(chloroquine,CQ)對H1688和H446細胞的生長抑制作用;免疫熒光法觀察自噬標記物LC3表達,示蹤自噬體形成;Western blot檢測自噬相關蛋白LC3及Akt/m TOR信號通路的表達。結(jié)果 AN呈濃度依賴性抑制H1688和H446細胞增殖并促進其死亡(P0.05);AN處理組可以顯著增加H1688和H446細胞自噬小體數(shù)量并誘導LC3-Ⅱ表達;自噬抑制劑CQ提高AN對H1688和H446細胞殺傷作用(P0.05);AN作用H1688細胞后p-Akt、p-m TOR、p-70S6K蛋白表達降低。結(jié)論 AN對小細胞肺癌H1688和H446細胞具有抑制作用并誘導細胞保護性自噬,阻斷自噬可以增強AN對小細胞肺癌H1688和H446細胞的抗癌療效。
[Abstract]:Objective to study the anticancer effects of asparagase ANs on H1688 and H446 cells of small cell lung cancer and to investigate the function of autophagy in the anticancer process of an. Methods MTT assay and Trypan blue staining were used to detect the growth inhibition of H1688 and H446 cells by an alone or in combination with chloroquine CQ, and the expression of autophagy marker LC3 was observed by immunofluorescence assay. The expression of autophagy associated protein (LC3) and Akt/m TOR signal pathway was detected by Western blot. Results an inhibited the proliferation of H1688 and H446 cells in a concentration-dependent manner and promoted the proliferation of H1688 and H446 cells and induced the expression of LC3- 鈪,
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