姜黄素通过抑制HR通路增强PEO1卵巢癌细胞系对尼拉帕利的敏感性

Curcumin enhances the sensitivity of PEO1 ovarian cancer cell line to niraparib by inhibiting the homologous recombination repair pathway

摘要:

目的 在PEO1卵巢癌细胞系中探究姜黄素对尼拉帕利敏感性的影响及其作用机制。方法 分别通过CCK8试验、平板克隆和TUNEL法检测姜黄素和尼拉帕利联合用药对PEO1细胞增殖和凋亡的影响，通过RAD51 foci检测和Western blotting实验评估姜黄素对同源重组修复（HR）通路的影响及机制。结果 姜黄素和尼拉帕利联合用药可显著抑制PEO1细胞增殖并促进其凋亡；姜黄素可显著增加PEO1细胞对尼拉帕利的敏感性，同时显著降低RAD51蛋白表达水平，抑制HR通路的功能。结论 姜黄素可通过下调RAD51蛋白表达抑制HR通路，从而提高PEO1卵巢癌细胞系对尼拉帕利的敏感性。

Abstract:

Objective To investigate the effects and mechanisms of curcumin on the sensitivity of PEO1 ovarian cancer cell line to niraparib.Methods The effects of curcumin and niraparib combination treatment on PEO1 cell proliferation and apoptosis were assessed using CCK8 assay, colony formation assay, and TUNEL assay, respectively. The impact of curcumin on the homologous recombination repair (HR) pathway and its mechanism were evaluated via RAD51 foci detection and Western blotting.Results The combination of curcumin with niraparib significantly inhibited PEO1 cell proliferation and promoted apoptosis. Curcumin enhanced the sensitivity of PEO1 cells to niraparib, accompanied by a marked reduction in RAD51 protein expression and suppression of HR pathway functionality.Conclusion Curcumin increased the sensitivity of PEO1 ovarian cancer cell line to niraparib by downregulating the RAD51 protein expression and inhibiting the HR pathway.