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Specific expression of lncRNA RP13-650J16.1 and TCONS_00023979 in prostate cancer
Author(s) -
Xiaochen Zhou,
Qiong Chen,
Haolin Wang,
Cheng Zhang,
Bin Fu,
Gongxian Wang
Publication year - 2018
Publication title -
bioscience reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.938
H-Index - 77
eISSN - 1573-4935
pISSN - 0144-8463
DOI - 10.1042/bsr20171571
Subject(s) - du145 , transfection , gene silencing , cancer research , clonogenic assay , prostate cancer , chemistry , microbiology and biotechnology , clone (java method) , biology , cancer , lncap , cell , gene , biochemistry , genetics
The aim of the present study was to explore the expression profile and the potential regulatory mechanism of two long non-coding RNAs (lncRNAs) (RP13-650J16.1 and TCONS_00023979) in prostate cancer (PCa). Expression profile of lncRNAs in PCa and paracancerous tissues were investgated by the high-throughput gene chip technology. Specific siRNA of RP13-650J16.1 or TCONS_00023979 was transfected into DU145 cells. Then, the relative expression of RP13-650J16.1, receptor-associated coactivator 3 (RAC3), promyelocytic leukemia (PML), and TCONS_00023979 was detected by quantitative real-time PCR and Western blotting. MTT assay was used to detect the proliferation of DU145 cells. The migration ability of DU145 cells was measured by Transwell chambers. Single cell proliferation and clonogenic ability were detected by plate clone formation assay. RP13-650J16.1 and RAC3 expression was up-regulated, and TCONS_00023979 and PML expression was down-regulated in PCa tissues. Silencing RP13-650J16.1 could decrease RAC3 expression, and knockout of TCONS_00023979 also reduced PML expression. Moreover, the ability of proliferation, migration, and colony formation of DU145 cells was decreased after transfected with si-RP13-650J16.1, while these abilities were increased after transfected with si-TCONS_00023979. Collectively, our findings demonstrated that RP13-650J16.1 might be an oncogene and TCONS_00023979 might be an antioncogene in PCa.

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