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. 2020 Mar 11;12(3):655. doi: 10.3390/cancers12030655

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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The scheme for molecular mechanisms of BNIP3L-dependent mitophagy-mediated reprogramming of glycolytic metabolism promoted cancer stemness in HBx-expressing HCC cells. In vivo, HBx-expressing promoted xenografted tumor growth, upregulated the expression of liver cancer stemness and BNIP3L-dependent mitophagy-related proteins, and increased the glycolytic metabolism. In vitro, HBx upregulated glycolysis metabolism reprogramming through BNIP3L-dependent mitophagy, and consequently enhanced the hepatic cancer stemness phenotypes in multiple HBx-expressing HCC cell models.