Effect of carboplatin combined with PF-04691502 on triple-negative breast cancer cell lines

唐小飞; 董志; 傅洁民; 曾凡新; 姜立花

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Effect of carboplatin combined with PF-04691502 on triple-negative breast cancer cell lines

更新时间：2026-01-09

- Effect of carboplatin combined with PF-04691502 on triple-negative breast cancer cell lines
- Journal of Army Medical University Vol. 35, Issue 5, Pages: 442-446(2013)
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  CLC： R737.9;R965;R979.1
- Published：2013
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唐小飞,董志,傅洁民,曾凡新,姜立花.卡铂联合PF-04691502抗三阴性乳腺癌细胞的体外研究[J].陆军军医大学学报(原第三军医大学学报),2013,35(05):442-446.

　Tang Xiaofei,Dong Zhi,Fu Jiemin,Zeng Fanxin,Jiang Lihua.Effect of carboplatin combined with PF-04691502 on triple-negative breast cancer cell lines[J].J Amry Med Univ (J Third Mil Med Univ),2013,35(05):442-446.
唐小飞,董志,傅洁民,曾凡新,姜立花.卡铂联合PF-04691502抗三阴性乳腺癌细胞的体外研究[J].陆军军医大学学报(原第三军医大学学报),2013,35(05):442-446. DOI：

　Tang Xiaofei,Dong Zhi,Fu Jiemin,Zeng Fanxin,Jiang Lihua.Effect of carboplatin combined with PF-04691502 on triple-negative breast cancer cell lines[J].J Amry Med Univ (J Third Mil Med Univ),2013,35(05):442-446. DOI：

摘要

目的研究卡铂与磷脂酰肌醇3-激酶（phosphoinositide 3-kinase

PI3K）抑制剂PF-04691502(PF)联合抗人三阴性乳腺癌(triple-negative breast cancer

TNBC)细胞的作用。方法通过细胞增殖实验、克隆形成实验、细胞划痕愈合实验以及流式细胞技术来分析卡铂和PF对TNBC细胞(HCC1937和MDA-MB 231)的抑制作用，并通过ELISA实验来检测PF对肿瘤发生过程中的关键蛋白Akt磷酸化的抑制作用。结果细胞增殖实验发现卡铂与PF对TNBC细胞均有协同抑制作用(CI1)；还能有效地抑制TNBC细胞克隆的形成和迁移(P0.01)。ELISA实验发现PF对TNBC细胞Akt的磷酸化也具有一定的抑制作用，并且具有浓度依赖性。流式细胞结果显示PF对TNBC细胞G

期有阻滞作用，而卡铂为周期非特异性药物。结论卡铂联合PF具有协同抗TNBC细胞的作用；并提示化疗药物联合PI3K抑制剂也许能够提高TNBC的治疗效果，并减少化疗药物的给药剂量、降低毒副作用。

Abstract

Objective To study the synergistic effect of carboplatin combined with a PI3K inhibitor PF-04691502 (PF) on triple-negative breast cancer (TNBC) cell lines. Methods The effect of carboplatin and PF on TNBC cell lines (HCC1937 and MDA-MB 231) was measured by proliferation assay

colony formation assay

wound-healing assay and flow cytometry

respectively. The phosphorylation of Akt

which was a key protein in the progress of tumors

was detected by ELISA. Results Carboplatin and PF inhibited the proliferation

colony formation and migration of TNBC c

ell lines (P0.01)

and the phosphorylation of Akt in TNBC cells was also inhibited in a dose-dependent manner. Carboplatin combined with PF showed significantly synergistic effect in above assays (CI1). Flow cytometry results showed that PF could arrest the TNBC cells in G

phase

but carboplatin was non-specific for cell cycle. Conclusion Carboplatin combined with PF has synergistic anti-tumor effect on TNBC cell lines

suggesting that chemotherapy combined with PI3K inhibitor may effectively improve the therapeutic effect

reduce the dosage of chemotherapeutics and decrease side effects.

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