1. Disruption of xCT inhibits cell growth via the ROS/autophagy pathway in hepatocellular carcinoma
- Author
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Ming Yao, Chao Ge, Ning Tan, Taoyang Chen, Xianghuo He, Deshui Jia, Yingjun Zhao, Weijie Guo, Jinjun Li, Fangyu Zhao, Linhui Liang, and Zhenfeng Zhang
- Subjects
Cancer Research ,Programmed cell death ,Carcinoma, Hepatocellular ,Amino Acid Transport System y+ ,Mice, Nude ,Cell Growth Processes ,Biology ,Transfection ,Mice ,chemistry.chemical_compound ,In vivo ,Cell Line, Tumor ,Autophagy ,medicine ,Animals ,Humans ,RNA, Messenger ,neoplasms ,Mice, Inbred BALB C ,Cell growth ,Liver Neoplasms ,Glutathione ,medicine.disease ,Xenograft Model Antitumor Assays ,digestive system diseases ,In vitro ,Cell biology ,Sulfasalazine ,Oncology ,chemistry ,Gene Knockdown Techniques ,Hepatocellular carcinoma ,System X ,Female ,Reactive Oxygen Species - Abstract
xCT, the functional subunit of the system x(c)(-) which plays an important role in maintaining intracellular glutathione (GSH) levels, is expressed in various malignant tumors. Here, we demonstrated that xCT expression is often elevated in HCC and is associated with poor prognosis in HCC patients; moreover, disruption of xCT suppressed HCC cell growth both in vitro and in vivo. xCT dysfunction has also been shown to increase intracellular reactive oxygen species (ROS) levels, thus in turn led to autophagic cell death of HCC cells. Taken together, these findings suggest that xCT may be a promising therapeutic target for human HCC.
- Published
- 2011
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