基础医学与临床 ›› 2021, Vol. 41 ›› Issue (7): 1018-1023.

• 研究论文 • 上一篇    下一篇

安罗替尼联合氯喹促进人非小细胞肺癌细胞系H1299凋亡

刘细帮1,朱林芝2,焦德敏1,唐夏莉1,陈君1,胡旭钢1,陈清勇2   

  1. 1. 中国人民解放军联勤保障部队第九〇三医院
    2. 温州医科大学第一临床医学院
  • 收稿日期:2020-07-24 修回日期:2020-11-04 出版日期:2021-07-05 发布日期:2021-06-17
  • 通讯作者: 陈清勇 E-mail:cqyong117@163.com
  • 基金资助:
    浙江省医药卫生科技计划项目;北京医卫健康公益基金

Anlotinib combined with chloroquine induces apoptosis of human non-small cell lung cancer cell line H1299

  • Received:2020-07-24 Revised:2020-11-04 Online:2021-07-05 Published:2021-06-17

摘要: 目的 探讨安罗替尼和氯喹(CQ)单用及联用对人非小细胞肺癌系H1299存活率、迁移、侵袭和凋亡的影响。方法 安罗替尼与CQ单用及两药联合处理H1299细胞,MTT法检测细胞的存活率;划痕愈合和Transwell小室法检测细胞迁移及侵袭能力;Hoechst 33342染色检测细胞凋亡;Western blot检测自噬标志物LC3-II/LC3-I和自噬底物p62蛋白表达。结果 安罗替尼联合CQ组对H1299细胞存活率、侵袭及迁移抑制效应优于安罗替尼组(P<0.05);安罗替尼单用时较对照组的细胞凋亡增加,当安罗替尼联合CQ作用时细胞凋亡增加更显著。安罗替尼随浓度增加明显上调自噬标志物蛋白LC3-II/LC3-I和下调自噬底物蛋白p62;CQ可显著上调LC3-II/LC3-I和p62表达水平;与单用CQ组相比,20 μmol/L安罗替尼联合CQ组更加显著上调LC3-II/LC3-I和下调p62。结论 安罗替尼联合氯喹可显著抑制非小细胞肺癌H1299细胞的存活率、迁移和侵袭,促使细胞凋亡;其机制可能通过自噬发挥抗肿瘤作用。

关键词: 关键词:NSCLC, 安罗替尼, 氯喹, 自噬, 凋亡

Abstract: Objective To investigate the effects of anlotinib and chloroquine (CQ) on viability, invasion and apoptosis of H1299 cells. Methods After H1299 cells were treated by anlotinib or/and CQ, the cell viability was measured by MTT assay; Wound-healing and transwell chamber assay were used to evaluate cell migration and invasion abilities; Hoechst 33342 staining was adopted to test the changes of apoptosis; The protein levels of autophagy marker LC3-II/LC3-I and autophagic substrate p62 were detected by western blotting. Results Anlotinib combined with CQ showed more obviously synergistic inhibitory effect on the viability, invasion and migration in H1299 cells than anlotinib alone (P<0.05). As compared to the untreated control cells, anlotinib alone promoted the cell apoptosis. Their combination induced an even higher apoptosis in H1299 cells. With the increase of concentration, anlotinib significantly up-regulated autophagy marker protein LC3-II/LC3-I and down-regulated autophagic substrate protein p62.The expression levels of LC3-II/LC3-I and p62 were significantly up-regulated by CQ. Compared with the CQ group alone, LC3-II /LC3-I and p62 were significantly up-regulated and down-regulated in the 20 μmol /L anlotinib combined with CQ group. Conclusions Combination of anlotinib and CQ remarkably inhibits the viability, migration and invasion and induces the apoptosis of H1299 cells. The potential mechanism for antitumor might be due to autophagy.

Key words: Key words:NSCLC, anlotinib, chloroquine, autophagy, apoptosis

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