期刊
ONCOLOGY LETTERS
卷 14, 期 6, 页码 7986-7992出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/ol.2017.7237
关键词
hepatocellular carcinoma; HOX transcript antisense RNA; cisplatin; multidrug resistance; ATP binding cassette subfamily B member 1; signal transducer and activator of transcription 3 signaling
类别
资金
- National Natural Science Foundation of China [81000889]
- Science and Technology Planning Project of Guangdong Province, China [2014A020212094]
- Natural Science Foundation of Guangdong Province, China [2016A030313218]
- Sun Yat-Sen Memorial Hospital [YXQH201704]
- Key Laboratory of Malignant Tumor Molecular Mechanism and Translational Medicine of Guangzhou Bureau of Science and Information Technology [(2013) 163]
- Key Laboratory of Malignant Tumor Gene Regulation and Target Therapy of Guangdong Higher Education Institutes [KLB09001]
Long non-coding RNA HOX transcript antisense RNA (HOTAIR) has been demonstrated to exhibit oncogenic activity in several types of cancer, including hepatocellular carcinoma (HCC). However, the association between HOTAIR and HCC multidrug resistance remains uncertain. The present study aimed to investigate the role of HOTAIR in HCC chemoresistance; it was found that knockdown of HOTAIR expression in HCC Huh7 cells resulted in decreased cell proliferation and increased chemosensitivity to cisplatin. Furthermore, expression levels of ATP binding cassette subfamily B member 1 (ABCB1) mRNA and protein were decreased in Huh7 cells upon HOTAIR-knockdown. In addition, HOTAIR-knockdown reduced the levels of phosphorylated signal transducer and activator of transcription 3 (STAT3), and inhibition of STAT3 phosphorylation reduced HOTAIR-mediated ABCB1 expression. Together, these findings indicated that knockdown of HOTAIR in Huh7 cells decreased STAT3 activity and ABCB1 expression, and increased chemosensitivity to cisplatin. Thus HOTAIR could serve as a novel potential therapeutic target to reverse multidrug resistance in HCC.
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