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Please use this identifier to cite or link to this item: http://hdl.handle.net/10564/3071

Title: Syndecan-1 responsive microRNA-126 and 149 regulate cell proliferation in prostate cancer.
Other Titles: Syndecan-1を介したmicroRNA-126および149は前立腺癌における細胞増殖を制御する
Authors: Fujii, Tomomi
Shimada, Keiji
Tatsumi, Yoshihiro
Fujimoto, Kiyohide
Konishi, Noboru
藤井, 智美
島田, 啓司
辰巳, 佳弘
藤本, 清秀
小西, 登
Keywords: MicroRNA
Syndecan-1
MiR-126
MiR-149
Prostate cancer
Issue Date: Jan-2015
Publisher: Elsevier
Citation: Biochemical and biophysical research communications Vol.456 No.1 p.183-189(2015.01)
Abstract: MicroRNAs (miRNAs) are short (19–24 nt), low molecular weight RNAs that play important roles in the regulation of target genes associated with cell proliferation, differentiation, and development, by binding to the 3′-untranslated region of the target mRNAs. In this study, we examined the expression of miRNA-126 (miR-126) and miR-149 in prostate cancer, and investigated the molecular mechanisms by which they affect syndecan-1 in prostate cancer. Functional analysis of miR-126 and miR-149 was conducted in the prostate cancer cell lines, PC3, Du145, and LNCaP. The expression levels of SOX2, NANOG, Oct4, miR-126 and miR-149 were evaluated by quantitative RT-PCR. After silencing syndecan-1, miR-126, and/or miR-149 in the PC3 cells, cell proliferation, senescence, and p21 induction were assessed using the MTS assay, senescence-associated β-galactosidase (SA-β-Gal) assay, and immunocytochemistry, respectively. Compared to the Du145 and LNCaP cells, PC3 cells exhibited higher expression of syndecan-1. When syndecan-1 was silenced, the PC3 cells showed reduced expression of miR-126 and miR-149 most effectively. Suppression of miR-126 and/or miR-149 significantly inhibited cell growth via p21 induction and subsequently, induced senescence. The mRNA expression levels of SOX2, NANOG, and Oct4 were significantly increased in response to the silencing of miR-126 and/or miR-149. Our results suggest that miR-126 and miR-149 are associated with the expression of syndecan-1 in prostate cancer cells. These miRNAs promote cell proliferation by suppressing SOX2, NANOG, and Oct4. The regulation of these factors by miR-126 and miR-149 is essential for syndecan-1-mediated development of androgen-refractory prostate cancer.
Description: 博士(医学)・乙第1358号・平成27年5月28日
Copyright © 2014 Elsevier Inc.
URI: http://hdl.handle.net/10564/3071
ISSN: 0006291X
Academic Degrees and number: 24601B1358
Degree-granting date: 2015-05-28
Degree name: 博士(医学)
Degree-granting institutions: 奈良県立医科大学
Appears in Collections:2015年度

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