阿法替尼与PF-04691502单用及联合对H1975细胞体外抗肿瘤作用研究

谭涵; 曾凡新; 姜立花; 董志; 傅洁民

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阿法替尼与PF-04691502单用及联合对H1975细胞体外抗肿瘤作用研究

论著 | 更新时间：2026-01-09

- 阿法替尼与PF-04691502单用及联合对H1975细胞体外抗肿瘤作用研究
- Anti-tumor effect of afatinib and PF-04691502 separately or combined on NSCLC H1975 cells in vitro
- 陆军军医大学学报 2014年36卷第12期页码：1291-1294
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  中图分类号： R734.2;R965;R979.1
- 纸质出版：2014
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谭涵,曾凡新,姜立花,董志,傅洁民.阿法替尼与PF-04691502单用及联合对H1975细胞体外抗肿瘤作用研究[J].陆军军医大学学报(原第三军医大学学报),2014,36(12):1291-1294.

　Tan Han,Zeng Fanxin,Jiang Lihua,Dong Zhi,Fu Jiemin.Anti-tumor effect of afatinib and PF-04691502 separately or combined on NSCLC H1975 cells in vitro[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(12):1291-1294.
谭涵,曾凡新,姜立花,董志,傅洁民.阿法替尼与PF-04691502单用及联合对H1975细胞体外抗肿瘤作用研究[J].陆军军医大学学报(原第三军医大学学报),2014,36(12):1291-1294. DOI：

　Tan Han,Zeng Fanxin,Jiang Lihua,Dong Zhi,Fu Jiemin.Anti-tumor effect of afatinib and PF-04691502 separately or combined on NSCLC H1975 cells in vitro[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(12):1291-1294. DOI：

摘要

目的研究Pan-HER不可逆抑制剂阿法替尼（Afatinib）和磷脂酰基醇3-激酶（phosphoinositide 3-kinase，PI3K）α抑制剂PF-04691502（PF）单用及联合对表皮生长因子受体（epidermal growth factor receptor，EGFR）抑制剂耐药的非小细胞肺癌（non-small cell lung cancer，NSCLC）细胞株H1975的体外抗肿瘤作用。方法通过MTS法、细胞划痕愈合实验、流式细胞术检测细胞周期和凋亡分析Afatinib和PF单药及联合对耐药性非小细胞肺癌细胞株H1975增殖、迁移等的影响。结果 Afatinib和PF单用对H1975细胞增殖有明显抑制作用，且抑制作用随浓度增加而加强；Afatinib和PF联合时对H1975细胞增殖、迁移均有明显协同抑制作用；Afatinib和PF单药和联合作用均主要使细胞阻滞在G

期（

0.05）；Afatinib和PF单用时较对照组的细胞凋亡率增加，且当两者联合作用时凋亡率增加更显著（

0.05）。结论 Pan-HER不可逆抑制剂Afatinib和PI3Kα抑制剂PF-04691502（PF）单用对耐药性非小细胞肺癌细胞株H1975有较强抑制作用，且当Afatinib和PF联合时对非小细胞肺癌细胞株H1975有协同抑制作用。

Abstract

Objective To study the anti-tumor effect of separated or combined application of Pan-HER irreversible inhibitor afatinib and phosphoinositide 3-kinase α (PI3Kα) inhibitor PF-04691502 on epidermal growth factor receptor (EGFR) inhibitor-resistant non-small cell lung cancer (NSCLC) H1975 cells in vitro. Methods Effects of afatinib and PF-04691502 (PF) separated or combined application on the proliferation and migration of H

1975 cells were analyzed by cell cycle and apoptosis with MTS assay

wound-healing assay

and flow cytometry. Results Afatinib and PF alone significantly inhibited the proliferation of H1975 cells in a dose-dependent manner. Afatinib combined with PF showed an evident synergetic inhibitory effect. Afatinib and PF separated or combined application both induced cell cycle arrest at G

phase (

0.05). As compared to the control group

afatinib and PF alone promoted cell apoptosis

and their combination induced a higher apoptotic rate of H1975 cells (

0.05). Conclusion Pan-HER irreversible inhibitor afatinib and PI3Kα inhibitor PF alone shows significant antitumor effects on drug-resistant NSCLC H1975 cells. Moreover

their combination exhibits synergistic anti-tumor effects.

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