Knockdown of long non-coding RNA HOTAIR sensitizes hepatocellular carcinoma cell to cisplatin by suppressing the STAT3/ABCB1 signaling pathway

• Published in: Oncology letters Vol. 14; no. 6; pp. 7986 - 7992
• Main Authors: Zhou, Jia-Jia, Cheng, Di, He, Xiao-Yu, Meng, Zhe, Ye, Hui-Lin, Chen, Ru-Fu
• Format: Journal Article
• Language: English
• Published: Greece D.A. Spandidos 01.12.2017; Spandidos Publications; Spandidos Publications UK Ltd
• Subjects: ATP binding cassette subfamily B member 1; Biotechnology; Breast cancer; Care and treatment; Chemotherapy; cisplatin; Cytokines; Development and progression; Drug resistance; Gene expression; Genetic aspects; Health aspects; Hepatocellular carcinoma; HOX transcript antisense RNA; Kinases; Liver cancer; Medical research; multidrug resistance; Multidrug resistant organisms; Oncology; Phosphatase; Phosphorylation; Proteins; signal transducer and activator of transcription 3 signaling; Studies; Transcription factors; HOX transcript antisense RNA; multidrug resistance; ATP binding cassette subfamily B member 1; signal transducer and activator of transcription 3 signaling; cisplatin; hepatocellular carcinoma
• ISSN: 1792-1074; 1792-1082
• DOI: 10.3892/ol.2017.7237

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.