GABARAPL1 acts as a potential marker and promotes tumor proliferation and metastasis in triple negative breast cancer
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Li Ran1, Tao Hong1, Xinhua Xiao1, Liming Xie2, Junlin Zhou1 and Gebo Wen1
1Department of Endocrine, The First Affiliated Hospital, University of South China, Hengyang, China
2Center for Gastric Cancer Research of Human Province, The First Affiliated Hospital, University of South China, Hengyang, China
Gebo Wen, email: email@example.com
Keywords: GABARAPL1, tumor marker, triple negative breast cancer, proliferation, invasion
Received: October 31, 2016 Accepted: June 04, 2017 Published: August 10, 2017
GABAA-receptor-associated protein like-1 (GABARAPL1) is involved in a variety of cancers. The purpose of this study was to investigate the expression, prognostic roles and functions of GABARAPL1 in triple negative breast cancer (TNBC). Quantitative real-time PCR (qRT-PCR) showed that GABARAPL1 was up regulated in both TNBC cell lines and clinical TNBC tissues. High GABARAPL1 expression level was associated with shorter overall survival (OS) and disease free survival (DFS). Furthermore, inhibition of GABARAPL1 suppressed cell proliferation, tumorigenesis, invasion and metastasis, and induced cell apoptosis. We found that metadherin (MTDH) was a downstream target of GABARAPL1. Inhibition of GABARAPL1 suppressed the mRNA and protein expression of MTDH, and overexpression of MTDH could reverse the effects of GABARAPL1 inhibition, which meant GABARAPL1 performed its function partly through MTDH. Our findings demonstrate that GABARAPL1 acts as a tumor promoter in TNBC partly through MTDH. Targeting at GABARAPL1 could be a potential therapeutic strategy for TNBC.
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