Elevated CXCL1 increases hepatocellular carcinoma aggressiveness and is inhibited by miRNA-200a
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Xiao Cui1,2,*, Zhao Li1,*, Jie Gao1, Peng-Ji Gao1, Yan-bing Ni1, Ji-Ye Zhu1
1Department of Hepatobilliary Surgery, Beijing Key Surgical Basic Research Laboratory of Liver Cirrhosis and Liver Cancer, Peking University People's Hospital, Beijing 100044, China
2Department of General Surgery, The Second Hospital of Anhui Medical University, Hefei 230601, China
*These authors contributed equally to this work
Ji-Ye Zhu, email: firstname.lastname@example.org
Keywords: CXCL1, carcinogenesis, hepatocellular carcinoma, miR-200a
Received: May 26, 2016 Accepted: August 09, 2016 Published: August 17, 2016
In this study, we investigated the value of measurement of the chemokine CXCL1 in clinical management of hepatocellular carcinoma (HCC) and its possible role in the molecular pathogenesis of HCC. High CXCL1 expression predicted recurrence in HCC patients and promoted tumor progression in both in vivo and in vitro experimental systems. Overexpression of CXCL1 increased mitochondrial metabolism and activated the epithelial-to-mesenchymal transition (EMT). Using computational analysis we identified the microRNA miR-200a as a putative post-transcriptional regulator of CXCL1. We found that levels of miR-200a were inversely correlated with CXCL1 expression in HCC patient tissue samples by northern blot and qRT-PCR. Furthermore, CXCL1 was identified as a direct target which was bound and inhibited by miR- 200a. These findings provide new insights into the role of CXCL1 in HCC and its post-transcriptional regulation and suggest it may be a prognostic indicator for poor outcomes and a potential target for therapy.
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