並列タイトル等microRNA-345の過剰発現は、MUC1およびTJP2の発現を抑制することにより、膵管腺癌細胞株の浸潤能に影響を及ぼす
一般注記type:Thesis
The majority of pancreatic carcinomas are pancreatic ductal adenocarcinomas (PDAC), and
the presence of non-invasive pancreatic intraepithelial neoplasia or intraductal papillary mucinous
neoplasm, as an associated lesion, is considered important. These microscopic hyperplastic or grossly
papillomatous lesions exhibit varying degrees of morphological atypia and may develop into invasive
carcinomas. In this study, we investigated whether mucin-1 (MUC1) is involved in the progression of
pancreatic carcinoma and examined the mechanisms by which microRNAs regulate MUC1 expression
in vitro. In PDAC cell lines, suppression of MUC1 expression reduced cell proliferation and invasion;
PDAC cell lines transfected with an miR-345 precursor suppressed the expression of MUC1, and
reduced cell proliferation and invasion. Tight junction protein 2 (TJP2), a putative target of miR-345,
is regulated by MUC1. The suppression of TJP2 expression reduced cell proliferation by inducing
apoptosis. These results suggest that MUC1 and TJP2, the putative target molecules of miR-345,
are critical in maintaining the invasive potential of pancreatic carcinoma cells, and regulating their
expression may prevent the progression of non-invasive pancreatic intraductal lesions to invasive
carcinomas. This study provides new insights for the development of novel molecular targeted
therapies for pancreatic carcinomas.
博士(医学)・甲第866号・令和5年3月15日
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This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
identifier:Applied Sciences Vol.12 No.11 Article No.5351 (2022 May)
identifier:http://ginmu.naramed-u.ac.jp/dspace/handle/10564/4098
identifier:Applied Sciences, 12(11): Article No.5351
連携機関・データベース国立情報学研究所 : 学術機関リポジトリデータベース(IRDB)(機関リポジトリ)
提供元機関・データベース奈良県立医科大学 : 奈良県立医科大学機関リポジトリ GINMU