Over-expression of ASIC1a promotes proliferation via activation of the β-catenin/LEF-TCF axis and is associated with disease outcome in liver cancer

Cheng Jin; Feng-Lai Yuan; Yuan-Long Gu; Xia Li; Min-Feng Liu; Xiao-Min Shen; Bo Liu; Mao-Qun Zhu

doi:10.18632/oncotarget.10774

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Research Papers:

Over-expression of ASIC1a promotes proliferation via activation of the β-catenin/LEF-TCF axis and is associated with disease outcome in liver cancer

Cheng Jin _, Feng-Lai Yuan, Yuan-Long Gu, Xia Li, Min-Feng Liu, Xiao-Min Shen, Bo Liu and Mao-Qun Zhu

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Oncotarget. 2017; 8:25977-25988. https://doi.org/10.18632/oncotarget.10774

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Abstract

Cheng Jin1, Feng-Lai Yuan2, Yuan-Long Gu1, Xia Li2, Min-Feng Liu1, Xiao-Min Shen1, Bo Liu1, Mao-Qun Zhu1

1Department of Hepatobiliary Pancreatic Center, The Third Hospital Affiliated to Nantong University, Wuxi, 214041, Jiangsu, China

2Department of Research Institute, The Third Hospital Affiliated to Nantong University, Wuxi, 214041, Jiangsu, China

Correspondence to:

Cheng Jin, email: [email protected]

Keywords: ASIC1a, β-catenin, CRISPR/CAS9, liver cancer, proliferation

Received: February 16, 2016 Accepted: June 04, 2016 Published: July 22, 2016

ABSTRACT

Acid-sensing ion channels 1a (ASIC1a) has been reported to promote migration and invasion in liver cancer. However, the clinical significance and molecular mechanism of ASIC1a in liver cancer remain unknown. In the study, we found that ASIC1a is frequently up-regulated in liver cancer tissues. The over-expression of ASIC1a is associated with advanced clinical stage and poor prognosis. The pro-proliferative of ASIC1a is pH dependent. Knockout of ASIC1a by CRISPR/CAS9 inhibited liver cancer cell proliferation and tumorigenicity in vitro and in vivo through β-catenin degradation and LEF-TCF inactivation. Our results indicated a potential diagnostic marker and chemotherapeutic target for liver cancer.

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Research Papers:

Over-expression of ASIC1a promotes proliferation via activation of the β-catenin/LEF-TCF axis and is associated with disease outcome in liver cancer

Abstract