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三氧化二砷通过下调Bcl-2诱导胆囊癌细胞凋亡。

Arsenic trioxide induces gallbladder carcinoma cell apoptosis via downregulation of Bcl-2.

作者信息

Ai Zhilong, Lu Weiqi, Qin Xinyu

机构信息

Zhongshan Hospital, Fudan University, Shanghai 200032, People's Republic of China.

出版信息

Biochem Biophys Res Commun. 2006 Sep 29;348(3):1075-81. doi: 10.1016/j.bbrc.2006.07.181. Epub 2006 Aug 7.

Abstract

Gallbladder carcinoma (GBC), an aggressive and mostly lethal malignancy, is known to be resistant to a number of apoptotic stimuli. Here, we report for the first time the pro-apoptosis role of arsenic trioxide (As2O3) in gallbladder carcinoma and identify the contribution of Bcl-2 in the As2O3-induced apoptosis. The treatment of As2O3 in gallbladder carcinoma cells could induce apoptosis in a dose-dependent manner and downregulate the expression of anti-apoptotic protein Bcl-2 at mRNA level. Moreover, Bcl-2 overexpression could protect gallbladder carcinoma cells from As2O3-induced apoptosis, indicating the contribution of Bcl-2 in As2O3-induced apoptosis. Taken together, these results suggest that arsenic trioxide induces gallbladder carcinoma cell apoptosis via downregulation of Bcl-2, which may have important therapeutic implications in gallbladder carcinoma patients.

摘要

胆囊癌(GBC)是一种侵袭性强且大多致命的恶性肿瘤,已知对多种凋亡刺激具有抗性。在此,我们首次报道三氧化二砷(As2O3)在胆囊癌中的促凋亡作用,并确定Bcl-2在As2O3诱导的凋亡中的作用。用As2O3处理胆囊癌细胞可呈剂量依赖性地诱导凋亡,并在mRNA水平下调抗凋亡蛋白Bcl-2的表达。此外,Bcl-2过表达可保护胆囊癌细胞免受As2O3诱导的凋亡,表明Bcl-2在As2O3诱导的凋亡中发挥作用。综上所述,这些结果表明三氧化二砷通过下调Bcl-2诱导胆囊癌细胞凋亡,这可能对胆囊癌患者具有重要的治疗意义。

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