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Post-translational modifiers of liver kinase B1/serine/threonine kinase 11 in hepatocellular carcinoma

Authors Delgado TC, Lopitz-Otsoa F, Martínez-Chantar ML

Received 4 January 2019

Accepted for publication 24 April 2019

Published 6 June 2019 Volume 2019:6 Pages 85—91


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Ahmed Kaseb

Video abstract of "Post-translational modifiers of LKB1 in HCC" [ID 169585].

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Teresa Cardoso Delgado, Fernando Lopitz-Otsoa, María Luz Martínez-Chantar

Liver Disease and Liver Metabolism Laboratories, CIC bioGUNE, Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Derio 48160, Bizkaia, Spain

Abstract: Liver kinase B1 (LKB1) also referred to as serine/threonine kinase 11 (STK11) encodes a 50 kDa evolutionary conserved serine/threonine kinase that is ubiquitously expressed in adult and fetal tissues. LKB1 is a master kinase known to phosphorylate and activate several kinases including AMP-activated protein kinase, a crucial cellular energy sensor. LKB1 shows pleiotropic activity playing diverse roles in multiple processes, including cell polarity and other processes relevant in cancer pathology, such as energy metabolism, proliferation and apoptosis. In spite of the fact that LKB1 is often considered a tumor suppressor in a wide variety of organs, in the last years, several studies have shown that LKB1 is unexpectedly high in hepatocellular carcinoma (HCC), the most common type of primary liver cancer. Post-translational modifications of LKB1 are potentially relevant in HCC. Herein, we provide a comprehensive revision of post-translational modifications of LKB1 in HCC and how they modulate LKB1 function by different mechanisms such as regulation of its activity, localization or stability. Overall, the signature post-translational modifications of LKB1 in HCC appear to play an important role in the rather unique role of LKB1 as an oncogenic driver in liver cancer and may provide an alternative valuable therapeutic approach to regulate LKB1 expression and/or activity in HCC.

Keywords: post-translational modifications, SUMO, NEDD8, STRADα, AMPK

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