NACC1, as a Target of MicroRNA-331-3p, Regulates Cell Proliferation in Urothelial Carcinoma Cells.

• Material Type: 博士論文
• Title: NACC1, as a Target of MicroRNA-331-3p, Regulates Cell Proliferation in Urothelial Carcinoma Cells.
• Author/Editor: Morita, Kohei; Fujii, Tomomi; Itami, Hiroe; Uchiyama, Tomoko; Nakai, Tokiko; Hatakeyama, Kinta; Sugimoto, Aya; Miyake, Makito; Nakai, Yasushi; Tanaka, Nobumichi; Shimada, Keiji; Yamazaki, Masaharu; Fujimoto, Kiyohide; Ohbayashi, Chiho
• Author Heading: Morita, Kohei; Fujii, Tomomi; Itami, Hiroe; Uchiyama, Tomoko; Nakai, Tokiko; Hatakeyama, Kinta; Sugimoto, Aya; Miyake, Makito; Nakai, Yasushi; Tanaka, Nobumichi; Shimada, Keiji; Yamazaki, Masaharu; Fujimoto, Kiyohide; Ohbayashi, Chiho
• Publication, Distribution, etc.: MDPI
• Publication Date: 2018-09-21
• Publication Date (W3CDTF): 2018-09-21
• Alternative Title: MicroRNA-331-3pはNACC1を標的とし、尿路上皮癌細胞の増殖を制御する
• Periodical title: Cancers
• No. or year of volume/issue: 10 10
• Volume: 10
• Issue: 10
• Pages: Article No.347-
• ISSN (Periodical Title): ISSN : 2072-6694
• Degree grantor/type: 奈良県立医科大学
• Date Granted: 2019-09-27
• Dissertation Number: 乙第1431号
• Degree Type: 博士（医学）
• Text Language Code: eng
• Subject Heading: urothelial carcinoma; NACC1; miR-331-3p; cell cycle arrest; migration and invasion
• Target Audience: 一般
• Note (General): type:Thesis; The nucleus accumbens-associated protein 1 (NACC1) is a transcription factor constitutively expressed in the urothelium, where it regulates cell growth, senescence, autophagy, and epithelial-mesenchymal transition. microRNA (miRNA) constitutes a class of small non-coding RNAs which are involved in cell proliferation, differentiation, and progression of tumors. miRNAs and their target molecules are utilized for molecular diagnosis of urothelial carcinoma. NACC1 is one of several putative target molecules of miR-331-3p, and is associated with cell proliferation in cancers such as prostate and cervical cancer. Functional experiments involving miR-331-3p and its target molecule NACC1 were conducted using the urothelial carcinoma (UC) cell lines, T24, UMUC6, and KU7. Furthermore, quantitative reverse transcription polymerase chain reaction and immunostaining were performed to evaluate the expression of NACC1 in UC derived from transurethral resection of bladder tumor (TUR-Bt) specimens. The methane thiosulfonate (MTS) assay revealed that cell proliferation was significantly reduced after transient transfection of miR-331-3p precursor and/or NACC1 siRNA in UC cells. Cell senescence via cell cycle arrest at the G1 phase was induced by NACC1 inhibition. On the other hand, suppression of NACC1 induced cell migration and invasion abilities. Immunohistochemical analysis of TUR-Bt specimens revealed that over 70% of UC cells presented strongly positive results for NACC1. In contrast, normal urothelial cells were weakly positive for NACC1. It was also found that NACC1 expression was lower in invasive UC cells than in non-invasive UC cells. Loss of NACC1 induced vessel invasion in invasive UC tissues. The present results indicate that NACC1 regulated by miR-331-3p contributes to cell proliferation, and is involved in cell migration and invasion. This suggests that NACC1 can serve as a potential target molecule for the prediction and prognosis of UC, and can contribute to effective treatment strategies.; 博士（医学）・乙第1431号・令和元年9月27日; © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).; identifier:Cancers Vol.10 No.10 Article No.347 (2018 Sep); identifier:20726694; identifier:http://ginmu.naramed-u.ac.jp/dspace/handle/10564/3667; identifier:Cancers, 10(10): Article No.347
• Access Restrictions: インターネット公開
• Related Material (DOI): 10.3390/cancers10100347
• Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）; https://irdb.nii.ac.jp
• Original Data Provider (Database): 奈良県立医科大学 : 奈良県立医科大学機関リポジトリ GINMU

Table of Contents

http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/3667/1/01%e4%b9%991431%e6%9c%ac%e6%96%87%e3%81%ae%e8%a6%81%e6%97%a8.pdf fulltext

http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/3667/2/02%e4%b9%991431%e5%af%a9%e6%9f%bb%e8%a6%81%e6%97%a8.pdf fulltext

http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/3667/3/03%e4%b9%991431%e6%9c%ac%e6%96%87.pdf fulltext

http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/3667/4/04%e4%b9%991431Supplementary%20Material.pdf fulltext