Functional and Clinical Evidence That TAZ is a Candidate Oncogene in Hepatocellular Carcinoma. Issue 11 (9th September 2015)

• Record Type: Journal Article
• Authors: Guo, Yan; Pan, Qiao; Zhang, Jing; Xu, Xinyuan; Liu, Xiping; Wang, Qinhao; Yi, Ru; Xie, Xiaobo; Yao, Libo; Liu, Wenchao; Shen, Lan
• Is Part Of: Journal of cellular biochemistry. Volume 116:Issue 11(2015:Nov.)
• Page Start: 2465
• Page End: 2475
• Publication Date: 2015-09-09
• Subjects: Cytochemistry -- Periodicals; 572
• DOI: 10.1002/jcb.25117
• Languages: English
• ISSNs: 0730-2312

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>ABSTRACT</title> <sec id="jcb25117-sec-0001" sec-type="section"> <p>Transcriptional co‐activator with PDZ‐binding motif (TAZ) has been reported to be associated with carcinogenesis. However, the cellular function of TAZ in human hepatocellular carcinoma (HCC) remains elusive. In this study, an immunohistochemistry analysis revealed that the expression of TAZ in cancer tissue samples from 180 HCC patients was significantly higher than that in adjacent normal tissues. In addition, TAZ overexpression was significantly correlated with aggressive tumor characteristics such as tumor size, TNM stage, lymph node or distant metastasis, histological differentiation, and recurrent HCC (<italic>P</italic> < 0.05). The Kaplan–Meier test showed that TAZ‐positive expression was related to a poor prognosis compared to TAZ‐negative expression (<italic>P</italic> < 0.05). Furthermore, the expression level of TAZ was generally correlated with the invasiveness of cancer cells. The overexpression of TAZ in the Huh7 cell line, which endogenously expresses TAZ at low levels, significantly promoted cell proliferation, migration and invasion and inhibited apoptosis, whereas RNA interference‐mediated knockdown of TAZ in the highly invasive cell line MHCC‐97H significantly suppressed cell proliferation, migration and invasion in vitro and tumor formation in vivo. J. Cell. Biochem. 116: 2465–2475, 2015. © 2015 Wiley Periodicals, Inc.</p> </sec> </abstract>