Research Papers:
Downregulation of LncRNA GAS5 causes trastuzumab resistance in breast cancer
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Abstract
Wentong Li1, Limin Zhai1, Hui Wang2, Chuanliang Liu3, Jinbao Zhang4, Weijuan Chen5, Qun Wei5
1Department of Pathology, Weifang Medical University, Weifang, Shandong Province, 261053, P.R. China
2Department of Oncology, People’s Hospital of Shouguang City, Shandong Province, 262700, P.R. China
3Department of Health Care, Weifang People’s Hospital, Weifang, Shandong Province, 261053, P.R. China
4Department of Molecular Genetics, Weifang Medical University, Weifang, Shandong Province, 261053, P.R. China
5Department of Pathology, People’s Hospital of Shouguang City, Shandong Province, 262700, P.R. China
Correspondence to:
Wentong Li, e-mail: [email protected]
Keywords: trastuzumab, lapatinib, drug resistance, lncRNA GAS5, mTOR
Received: January 28, 2016 Accepted: March 16, 2016 Published: March 28, 2016
ABSTRACT
Therapeutic resistance to trastuzumab caused by dysregulation of long noncoding RNAs (lncRNAs) is a major obstacle to clinical management of HER2-positive breast cancer. To investigate which lncRNAs contribute to trastuzumab resistance, we screened a microarray of lncRNAs involved in the malignant phenotype of trastuzumab-resistant SKBR-3/Tr cells. Expression of the lncRNA GAS5 was decreased in SKBR-3/Tr cells and in breast cancer tissue from trastuzumab-treated patients. Inhibition of GAS5 promoted SKBR-3 cell proliferation, and GAS5 knockdown partially reversed lapatinib-induced inhibition of SKBR-3/Tr cell proliferation. GAS5 suppresses cancer proliferation by acting as a molecular sponge for miR-21, leading to the de-repression of phosphatase and tensin homologs (PTEN), the endogenous target of miR-21. Moreover, mTOR activation associated with reduced GAS5 expression was required to suppress PTEN. This work identifies GAS5 as a novel prognostic marker and candidate drug target for HER2-positive breast cancer.
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