Kurabe N, Murakami S, Tashiro F. SGF29 and Sry pathway in hepatocarcinogenesis. World J Biol Chem 2015; 6(3): 139-147 [PMID: 26322172 DOI: 10.4331/wjbc.v6.i3.139]
Corresponding Author of This Article
Dr. Fumio Tashiro, Department of Biological Science and Technology, Faculty of Industrial Science and Technology, Tokyo University of Science, Niijuku 6-3-1, Katsushika-ku, Tokyo 125-8585, Japan. ftashir@rs.noda.tus.ac.jp
Research Domain of This Article
Oncology
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Biol Chem. Aug 26, 2015; 6(3): 139-147 Published online Aug 26, 2015. doi: 10.4331/wjbc.v6.i3.139
SGF29 and Sry pathway in hepatocarcinogenesis
Nobuya Kurabe, Shigekazu Murakami, Fumio Tashiro
Nobuya Kurabe, Department of Tumor Pathology, Hamamatsu University School of Medicine, Shizuoka 431-3192, Japan
Shigekazu Murakami, Fumio Tashiro, Department of Biological Science and Technology, Faculty of Industrial Science and Technology, Tokyo University of Science, Tokyo 125-8585, Japan
Author contributions: Kurabe N developed and wrote the manuscript; Murakami S and Tashiro F contributed to the design and editing of the paper; all authors approve the final version for submission.
Supported by The “Academic Frontier” project for Private University: a matching fund subsidy from MEXT (Ministry of Education, Culture, Sports, Science and Technology), 2006-2010 (to Tashiro F).
Conflict-of-interest statement: The authors declare no conflict of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Dr. Fumio Tashiro, Department of Biological Science and Technology, Faculty of Industrial Science and Technology, Tokyo University of Science, Niijuku 6-3-1, Katsushika-ku, Tokyo 125-8585, Japan. ftashir@rs.noda.tus.ac.jp
Telephone: +81-03-58761717 Fax: +81-03-58761639
Received: April 27, 2015 Peer-review started: April 29, 2015 First decision: May 14, 2015 Revised: May 31, 2015 Accepted: June 30, 2015 Article in press: July 2, 2015 Published online: August 26, 2015 Processing time: 120 Days and 14 Hours
Abstract
Deregulated c-Myc expression is a hallmark of many human cancers. We have recently identified a role of mammalian homolog of yeast SPT-ADA-GCN5-acetyltransferas (SAGA) complex component, SAGA-associated factor 29 (SGF29), in regulating the c-Myc overexpression. Here, we discuss the molecular nature of SFG29 in SPT3-TAF9-GCN5-acetyltransferase complex, a counterpart of yeast SAGA complex, and the mechanism through which the elevated SGF29 expression contribute to oncogenic potential of c-Myc in hepatocellularcarcinoma (HCC). We propose that the upstream regulation of SGF29 elicited by sex-determining region Y (Sry) is also augmented in HCC. We hypothesize that c-Myc elevation driven by the deregulated Sry and SGF29 pathway is implicated in the male specific acquisition of human HCCs.
Core tip: Deregulated c-Myc expression is a hallmark of many human cancers. We have recently identified a role of mammalian homolog of yeast SPT-ADA-GCN5-acetyltransferas (SAGA) complex component, SAGA-associated factor 29 (SGF29), in regulating the c-Myc overexpression. We propose that the upstream regulation of SGF29 elicited by sex-determining region Y (Sry) is also augmented in hepatocellularcarcinoma (HCC). We hypothesize that c-Myc elevation driven by the deregulated Sry and SGF29 pathway is implicated in the male specific acquisition of human HCCs.
