Knockdown of Hotair suppresses proliferation and cell cycle progression in hepatocellular carcinoma cell by downregulating CCND1 expression

被引:37
作者
Zhou, Jia-Jia [1 ]
Cheng, Di [1 ]
He, Xiao-Yu [2 ]
Meng, Zhe [1 ]
Li, Wen-Zhu [1 ]
Chen, Ru-Fu [1 ]
机构
[1] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Guangdong Prov Key Lab Malignant Tumor Epigenet &, 107 West Yan Jiang Rd, Guangzhou 510120, Guangdong, Peoples R China
[2] Guangdong Prov Inst Sports Sci, Lab Biomech & Physiol, Guangzhou 510663, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
hepatocellular carcinoma; homeobox transcript antisense RNA; proliferation; cell cycle; CCND1; gene; signal transducer and activator of transcription 3; LONG NONCODING RNA; CHROMATIN; STAT3; PHOSPHORYLATION; D1;
D O I
10.3892/mmr.2017.7162
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The long noncoding RNA, homeobox transcript antisense RNA (Hotair), has been demonstrated to have an important role in regulating various biological processes in various cancers, including hepatocellular carcinoma (HCC). However, the importance of Hotair in HCC proliferation and cell cycle progression remains to be elucidated. In the present study, knockdown of HOTAIR expression by RNA interference inhibited cell proliferation and induced G0/G1 cell cycle arrest in Huh7 hepatocellular carcinoma cells. In addition, the expression levels of CCND1 mRNA and its cyclin D1 protein product were reduced in Huh7 cells following knockdown of HOTAIR. Knockdown of HOTAIR reduced the expression of phosphorylated signal transducer and activator of transcription 3 (STAT3) and HOTAIR knockdown combined with STAT3 inhibition led to an additional decrease in cyclin D1 expression. The present study suggested that Hotair may have a critical role in the proliferation of HCC by regulating cell cycle, STAT3 activity and cyclin D1 expression. Therefore, Hotair may be a novel potential therapeutic target for HCC treatment.
引用
收藏
页码:4980 / 4986
页数:7
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