Long non-coding RNA BCYRN1 promotes prostate cancer progression via elevation of HDAC11

被引:29
|
作者
Huo, Wei [1 ]
Qi, Fei [2 ]
Wang, Kaichen [1 ]
机构
[1] Jilin Univ, China Japan Union Hosp, Dept Urol, 126 Xiantai Rd, Changchun 130033, Jilin, Peoples R China
[2] Jilin Univ, China Japan Union Hosp, Dept Surg, Changchun 130033, Jilin, Peoples R China
关键词
brain cytoplasmic RNA 1; histone deacetylase 11; prostate cancer; GENE-EXPRESSION; DEACETYLASE; 11; LNCRNA; PROLIFERATION; REPRESSION; RESISTANCE; MARKER; TARGET; CELLS;
D O I
10.3892/or.2020.7680
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Prostate cancer is a serious threat to men's health worldwide. While previous studies have demonstrated that long non-coding RNAs (lncRNAs) are closely associated with the initiation and development of several types of cancer, the role of lncRNAs in the progression of prostate cancer remains incompletely understood. In the present study, the lncRNA brain cytoplasmic RNA 1 (BCYRN1) was found to be overexpressed in prostate tumors compared with healthy tissues. Furthermore, the expression of BCYRN1 was found to be associated with Gleason score and lymph node metastasis. It was demonstrated that BCYRN1 silencing using small interfering RNA (siRNA) inhibited the proliferation of prostate cancer cells. The results of the present study indicated the presence of a reciprocal regulatory association between BCYRN1 and microRNA (miR)-939-3p. In addition, it was observed that BCYRN1 directly sponged miR-939-3p to upregulate histone deacetylase 11 (HDAC11) expression in prostate cancer cells. Moreover, transfection of recombinant HDAC11 reversed the inhibition of cell proliferation that was induced by BCYRN1 siRNA. A positive correlation between BCYRN1 and HDAC11 mRNA expression levels was also identified in prostate tumor and healthy tissues. Therefore, the findings of the present study may provide novel insight into the effects of lncRNAs on prostate cancer, and may enable the development of new therapeutic methods for patients with prostate cancer.
引用
收藏
页码:1233 / 1245
页数:13
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