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2 results on '"Liver cancer stem cells"'

1. BNIP3L-Dependent Mitophagy Promotes HBx-Induced Cancer Stemness of Hepatocellular Carcinoma Cells via Glycolysis Metabolism Reprogramming

Author

Wei-Hua Wang, You Lan, Liyin Zhang, Deng-Lin Zhan, Yuchun Lin, Yuan-Yuan Chen, Lin Che, Zhongning Lin, and Zi-Yan Huang

Subjects
0301 basic medicine, Cancer Research, viruses, Biology, Mitochondrion, lcsh:RC254-282, Article, 03 medical and health sciences, BNIP3L, 0302 clinical medicine, Side population, Mitophagy, medicine, hepatitis B virus x protein, Cancer, medicine.disease, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, digestive system diseases, glycolysis metabolism reprogramming, HBx, 030104 developmental biology, mitophagy, Oncology, liver cancer stem cells, 030220 oncology & carcinogenesis, Cancer research, Stem cell, Liver cancer, Reprogramming
Abstract

Hepatitis B virus (HBV) is one of predisposing factors for hepatocellular carcinoma (HCC). The role of HBV x protein (HBx) in mediating the induction and maintenance of cancer stemness during HBV-related HCC attracts considerable attention, but the exact mechanism has not been clearly elucidated. Here, ABCG2-dependent stem-like side population (SP) cells, which are thought to be liver cancer stem cells (LCSCs), were present in HCC cells, and the fraction of this subset was increased in HBx-expressing HCC cells. In addition, glycolysis was upregulated in LCSCs and HBx-expressing HCC cells, and intervention of glycolysis attenuated cancer stem-like phenotypes. Mitochondria play an important role in the maintenance of energy homeostasis, BNIP3L-dependent mitophagy was also activated in LCSCs and HBx-expressing HCC cells, which triggered a metabolic shift toward glycolysis. In summary, we proposed a positive feedback loop, in which HBx induced BNIP3L-dependent mitophagy which upregulated glycolytic metabolism, increasing cancer stemness of HCC cells in vivo and in vitro. BNIP3L might be a potential therapeutic target for intervention of LCSCs-associated HCC. Anti-HBx, a monoclonal antibody targeting intracellular HBx, had the potential to delay the progression of HBV infection related-HCC.

Published
2020

2. BNIP3L-Dependent Mitophagy Promotes HBx-Induced Cancer Stemness of Hepatocellular Carcinoma Cells via Glycolysis Metabolism Reprogramming.

Author

Chen, Yuan-Yuan, Wang, Wei-Hua, Che, Lin, Lan, You, Zhang, Li-Yin, Zhan, Deng-Lin, Huang, Zi-Yan, Lin, Zhong-Ning, and Lin, Yu-Chun

Subjects
*ANTINEOPLASTIC agents, *THERAPEUTIC use of monoclonal antibodies, *ANIMAL experimentation, *GENE expression, *GLYCOLYSIS, *HEPATITIS B, *HEPATOCELLULAR carcinoma, *HOMEOSTASIS, *MICE, *MITOCHONDRIA, *STEM cells, *PHENOTYPES, *DISEASE progression, *SIGNAL peptides, *IN vitro studies, *IN vivo studies, *DISEASE complications, *DISEASE risk factors
Abstract

Hepatitis B virus (HBV) is one of predisposing factors for hepatocellular carcinoma (HCC). The role of HBV x protein (HBx) in mediating the induction and maintenance of cancer stemness during HBV-related HCC attracts considerable attention, but the exact mechanism has not been clearly elucidated. Here, ABCG2-dependent stem-like side population (SP) cells, which are thought to be liver cancer stem cells (LCSCs), were present in HCC cells, and the fraction of this subset was increased in HBx-expressing HCC cells. In addition, glycolysis was upregulated in LCSCs and HBx-expressing HCC cells, and intervention of glycolysis attenuated cancer stem-like phenotypes. Mitochondria play an important role in the maintenance of energy homeostasis, BNIP3L-dependent mitophagy was also activated in LCSCs and HBx-expressing HCC cells, which triggered a metabolic shift toward glycolysis. In summary, we proposed a positive feedback loop, in which HBx induced BNIP3L-dependent mitophagy which upregulated glycolytic metabolism, increasing cancer stemness of HCC cells in vivo and in vitro. BNIP3L might be a potential therapeutic target for intervention of LCSCs-associated HCC. Anti-HBx, a monoclonal antibody targeting intracellular HBx, had the potential to delay the progression of HBV infection related-HCC. [ABSTRACT FROM AUTHOR]

Published
2020
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