p62, Upregulated during Preneoplasia, Induces Hepatocellular Carcinogenesis by Maintaining Survival of Stressed HCC-Initiating Cells

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p62, Upregulated during Preneoplasia, Induces Hepatocellular Carcinogenesis by Maintaining Survival of Stressed HCC-Initiating Cells

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作者：Atsushi Umemura¹ ; ⁵ ; Feng He¹ ; Koji Taniguchi¹ ; ¹⁰ ; ¹¹ ; Hayato Nakagawa¹ ; ⁷ ; Shinichiro Yamachika¹ ; Joan Font-Burgada¹ ; Zhenyu Zhong¹ ; Shankar Subramaniam³ ; Sindhu Raghunandan³ ; Angeles Duran⁹ ; Juan F. Linares⁹ ; Miguel Reina-Campos⁹ ; Shiori Umemura¹ ; ⁶ ; Mark A. Valasek² ; Ekihiro Seki⁴ ; ⁸ ; Kanji Yamaguchi⁵ ; Kazuhiko Koike⁷ ; Yoshito Itoh⁵ ; Maria T. Diaz-Meco⁹ ; Jorge Moscat⁹ ; ^{jmoscat@sbpdiscovery.org" class="auth_mail" title="E-mail the corresponding author} ; Michael Karin¹ ; ² ; ^{karinoffice@ucsd.edu" class="auth_mail" title="E-mail the corresponding author}
刊名：Cancer Cell
出版年：2016
出版时间：13 June 2016
年：2016
卷：29
期：6
页码：935-948
全文大小：7051 K

文摘

•: p62 in preneoplastic lesions is important for HCC development regardless of etiology
•: Ectopic p62 expression is sufficient for HCC induction in autophagy-competent liver
•: p62 exerts its oncogenic activity via NRF2 and mTORC1 but not via ubiquitin binding
•: p62 promotes survival and expansion of ROS-containing HCC-initiating cells

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