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Knockdown of ribosomal protein S15A inhibits proliferation of breast cancer cells through induction of apoptosis in vitro

机译:敲低核糖体蛋白S15A通过诱导体外细胞凋亡来抑制乳腺癌细胞的增殖

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摘要

To explore the role of ribosomal protein S15A (RPS15A) in breast cancer. The Oncomine database was used to compare the expression of RPS15A in human breast cancer tissues and normal tissues. RPS15A in breast cancer cell line ZR-75-30 and BT474 was specifically knocked down using lentivirus-mediated short hairpin RNAs (shRNAs). RPS15A knockdown efficiency was validated by quantitative polymerase chain reaction and western blot analysis. Subsequently, the functional effects of RPS15A on proliferation of breast cancer cells were investigated by MTT, colony formation and flow cytometry assays. Functional analysis indicated that RPS15A knockdown could inhibit cell proliferation, induced cell cycle arrest and apoptosis. Mechanism analysis revealed RPS15A mediated apoptosis via activating of caspase-3 and PARP cleavage, upregulating of Bad and BAX and downregulating of Bcl-2. Our preliminary study highlighted the importance of RPS15A in breast cancer growth. The inhibition of RPS15A may be a promising therapeutic target for breast cancer treatment.
机译:探讨核糖体蛋白S15A(RPS15A)在乳腺癌中的作用。Oncomine 数据库用于比较 RPS15A 在人乳腺癌组织和正常组织中的表达。使用慢病毒介导的短发夹 RNA (shRNA) 特异性敲低乳腺癌细胞系 ZR-75-30 和 BT474 中的 RPS15A。通过定量聚合酶链反应和蛋白质印迹分析验证了RPS15A的敲低效率。随后,通过MTT、集落形成和流式细胞术研究了RPS15A对乳腺癌细胞增殖的功能影响。功能分析表明,敲低RPS15A可抑制细胞增殖,诱导细胞周期停滞和细胞凋亡。机理分析显示,RPS15A通过激活caspase-3和PARP裂解、上调Bad和BAX以及下调Bcl-2介导细胞凋亡。我们的初步研究强调了RPS15A在乳腺癌生长中的重要性。抑制RPS15A可能是乳腺癌治疗的一个有前途的治疗靶点。

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