Overexpression of LAPTM4B-35 promotes growth and metastasis of hepatocellular carcinoma in vitro and in vivo

Yang, Hua; Xiong, Fuxia; Wei, Xuanhui; Yang, Yu; McNutt, Michael A.; Zhou, Rouli

doi:10.1016/j.canlet.2010.02.006

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Volume 294, Issue 2 , Pages 236-244, 28 August 2010

Overexpression of LAPTM4B-35 promotes growth and metastasis of hepatocellular carcinoma in vitro and in vivo

Hua Yang
- Department of Cell Biology, School of Basic Medical Sciences, Peking University, Beijing 100191, China
- These authors contributed equally to this work.
Fuxia Xiong
- Department of Cell Biology, School of Basic Medical Sciences, Peking University, Beijing 100191, China
- These authors contributed equally to this work.
Xuanhui Wei
- Department of Cell Biology, School of Basic Medical Sciences, Peking University, Beijing 100191, China
Yu Yang
- Department of Pathology, School of Basic Medical Sciences, Peking University, Beijing, China
Michael A. McNutt
- Department of Pathology, School of Basic Medical Sciences, Peking University, Beijing, China
Rouli Zhou
- Department of Cell Biology, School of Basic Medical Sciences, Peking University, Beijing 100191, China
- Corresponding author. Tel.: +86 10 82801468; fax: +86 10 6235 8270.

Received 16 December 2009; received in revised form 5 February 2010; accepted 10 February 2010. published online 04 March 2010.

Abstract

LAPTM4B-35, encoded by Lysosomal protein transmembrane 4 beta (LAPTM4B) is over-expressed in more than 71% of hepatocellular carcinomas (HCCs) and associated with prognosis of the patients. But the exact role and molecular mechanism in HCC have not been determined. In this study, we explored the effects and mechanisms of LAPTM4B-35 on tumor growth and metastasis in vitro and in vivo by overexpression and depletion of LAPTM4B in HCC HepG2 and Bel7402 cells. These findings suggest that overexpression of LAPTM4B-35 plays a critical role in the growth and metastasis of HCC, and LAPTM4B-35 may therefore be a therapeutic target for HCC.

Keywords: LAPTM4B-35, HCC, Tumorigenesis, Cell cycle, AKT