CAS调节乳腺癌细胞MDA-MB-231增殖和转移的研究

CAS regulates the proliferation and metastasis in the MDA-MB-231 breast cancer cells

为阐明细胞凋亡易感因子(CAS)在三阴性乳腺癌发生发展中的作用,通过siRNA转染构建敲减CAS的MDA-MB-231细胞模型,荧光定量PCR和蛋白质印迹验证CAS的敲除效率。随后利用CCK8试剂盒检测细胞活力:利用CellEventTM Caspase-3/7 Green ReadyProbes^(TM) Reagent试剂盒检测细胞的凋亡情况;利用Transwell试验评价细胞的迁移和侵袭能力来研究CAS基因对三阴性乳腺癌细胞(MDA-MB-231)的影响。结果表明:CAS在三阴性乳腺癌中呈现高表达,敲减CAS表达能显著降低MDA-MB-231的细胞活力,增加细胞凋亡率。细胞迁移和侵袭试验结果表明,敲减CAS可显著抑制MDA-MB-231细胞的迁移与侵袭能力。综合而言,CAS低表达可显著抑制乳腺癌细胞MDA-MB-231的增殖、迁移和侵袭,从而影响三阴性乳腺癌的发生和发展。CAS有望成为三阴性乳腺癌治疗的潜在靶点。

To elucidate the role of cellular apoptosis susceptibility(CAS)in the development of triple-negative breast cancer,the interfering CAS gene was achieved by the siRNA targeting CAS in the MDA-MB-231 cells.The knockdown efficiency of CAS was examined by qPCR and Western blot analysis.Cell viability was evaluated by CCK8 assay and cell apoptosis was detected by CellEvent^(TM) Caspase-3/7 Green ReadyProbesTM Reagent.Cell migration and invasion assays were assessed by the transwell assay to investigate the effects of CAS on the triple negative breast cancer cell line MDA-MB-231.The results showed that CAS was highly expressed in triple-negative breast cancer and knockdown of CAS significantly reduced the viability of MDA-MB-231 cells.The cell apoptosis rate(%)was remarkably increased when the CAS was knockdown.Furthermore,cell migration and invasion capacity were significantly inhibited in the siCAS cells.In general,the deficiency of CAS significantly inhibited the breast cancer cell(MDA-MB-231)in the proliferation,migration and invasion,further to hamper the occurrence and development of triple negative breast cancer.The present study suggests that CAS might be a promising therapeutic target for TNBC.