DSpace About DSpace Software 日本語
 

GINMU >
01 奈良県立医科大学 >
012 大学院 >
0122 学位請求論文 >
01221 博士論文(医学) >
2019年度 >

Please use this identifier to cite or link to this item: http://hdl.handle.net/10564/3667

Title: NACC1, as a Target of MicroRNA-331-3p, Regulates Cell Proliferation in Urothelial Carcinoma Cells.
Other Titles: 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
Authors: 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
Keywords: urothelial carcinoma
NACC1
miR-331-3p
cell cycle arrest
migration and invasion
Issue Date: 21-Sep-2018
Publisher: MDPI
Citation: Cancers Vol.10 No.10 Article No.347 (2018 Sep)
Abstract: 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.
Description: 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/).
URI: http://hdl.handle.net/10564/3667
ISSN: 20726694
Academic Degrees and number: 24601B1431
Degree-granting date: 2019-09-27
Degree name: 博士(医学)
Degree-granting institutions: 奈良県立医科大学
Appears in Collections:2019年度

Files in This Item:

File Description SizeFormat
01乙1431本文の要旨.pdf乙1431本文の要旨1.49 MBAdobe PDFView/Open
02乙1431審査要旨.pdf乙1431審査要旨1.26 MBAdobe PDFView/Open
03乙1431本文.pdf乙1431本文4.89 MBAdobe PDFView/Open
04乙1431Supplementary Material.pdf乙1431Supplementary Material1.47 MBAdobe PDFView/Open

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

 

Valid XHTML 1.0! DSpace Software Copyright © 2002-2010  Duraspace - Feedback