Borax-induced apoptosis in HepG2 cells involves p53, Bcl-2, and Bax.
作者： Y. Wei , F.J. Yuan , W.B. Zhou , L. Wu , L. Chen
DOI: 10.4238/GMR.15028300
关键词:
摘要: Borax, a boron compound and salt of boric acid, is known to inhibit the growth tumor cells. HepG2 cells have been shown be clearly susceptible anti-proliferative effects borax. However, specific mechanisms regulating this effect are poorly understood. This study aimed investigate pathways underlying inhibition induced by borax in The on cell viability were characterized using MTT. Apoptosis was also verified annexin V/propidium iodide staining. JC-1 dye western blotting techniques used measure mitochondrial membrane potential p53, Bax, Bcl-2 protein expression, respectively. Relevant mRNA levels measured qRT-PCR. Borax inhibited proliferation time- dose-dependent manner vitro. apoptotic process triggered involved upregulation p53 Bax downregulation Bcl-2, which confirmed change potential. These results elucidate borax-induced pathway that involves Bcl-2.
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