title: Borax-induced apoptosis in HepG2 cells involves p53, Bcl-2, and Bax.
abstract: Borax, a boron compound and a salt of boric acid, is known to inhibit the growth of tumor cells. HepG2 cells have been shown to be clearly susceptible to the anti-proliferative effects of borax. However, the specific mechanisms regulating this effect are poorly understood. This study aimed to investigate the pathways underlying the growth inhibition induced by borax in HepG2 cells. The effects of borax on HepG2 cell viability were characterized using MTT. Apoptosis was also verified by annexin V/propidium iodide staining. JC-1 dye and western blotting techniques were used to measure mitochondrial membrane potential and p53, Bax, and Bcl-2 protein expression, respectively. Relevant mRNA levels were measured by qRT-PCR. Borax inhibited the proliferation of HepG2 cells in a time- and dose-dependent manner in vitro. The apoptotic process triggered by borax involved the upregulation of p53 and Bax and the downregulation of Bcl-2, which was confirmed by a change in the mitochondrial membrane potential. These results elucidate a borax-induced apoptotic pathway in HepG2 cells that involves the upregulation of p53 and Bax and the downregulation of Bcl-2.
authors.affiliation: Experiment Center of Medicine, DongFeng Hospital, Hubei University of Medicine, Shiyan, Hubei, China.
authors.forename: Y
authors.initials: Y
authors.lastname: Wei
authors.affiliation: Institute of Liver Surgery, DongFeng Hospital, Hubei University of Medicine, Shiyan, Hubei, China.
authors.forename: F J
authors.initials: FJ
authors.lastname: Yuan
authors.affiliation: Institute of Liver Surgery, DongFeng Hospital, Hubei University of Medicine, Shiyan, Hubei, China.
authors.forename: W B
authors.initials: WB
authors.lastname: Zhou
authors.affiliation: Institute of Liver Surgery, DongFeng Hospital, Hubei University of Medicine, Shiyan, Hubei, China.
authors.forename: L
authors.initials: L
authors.lastname: Wu
authors.affiliation: Experiment Center of Medicine, DongFeng Hospital, Hubei University of Medicine, Shiyan, Hubei, China.
authors.forename: L
authors.initials: L
authors.lastname: Chen
authors.affiliation: Experiment Center of Medicine, DongFeng Hospital, Hubei University of Medicine, Shiyan, Hubei, China.
authors.forename: J J
authors.initials: JJ
authors.lastname: Wang
authors.affiliation: Institute of Liver Surgery, DongFeng Hospital, Hubei University of Medicine, Shiyan, Hubei, China.
authors.forename: Y S
authors.initials: YS
authors.lastname: Zhang
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D001881:Borates / Q000494:pharmacology* / Q000633:toxicity; D054697:Cytostatic Agents / Q000494:pharmacology* / Q000633:toxicity; D015536:Down-Regulation; D056945:Hep G2 Cells; D006801:Humans; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism*; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism*
chemical_list: C494826:BAX protein, human; D001881:Borates; D054697:Cytostatic Agents; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53; D051028:bcl-2-Associated X Protein; C018851:borax