Research Papers:

GABARAPL1 acts as a potential marker and promotes tumor proliferation and metastasis in triple negative breast cancer

Li Ran, Tao Hong, Xinhua Xiao, Liming Xie, Junlin Zhou and Gebo Wen _

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Oncotarget. 2017; 8:74519-74526. https://doi.org/10.18632/oncotarget.20159

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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

Correspondence to:

Gebo Wen, email: wengb@nhu.edu.cn

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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