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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/44985
Title: Nc886 is induced by TGF-β and suppresses the microRNA pathway in ovarian cancer
Authors: Ji Hye Ahn
Hyun Sung Lee
Ju Seog Lee
Yeon Su Lee
Jong Lyul Park
Seon Young Kim
Jung Ah Hwang
Nawapol Kunkeaw
Sung Yun Jung
Tae Jin Kim
Kwang Soo Lee
Sung Ho Jeon
Inhan Lee
Betty H. Johnson
Jung Hye Choi
Yong Sun Lee
National Cancer Center, Gyeonggi
Korea Research Institute of Bioscience and Biotechnology
Hallym University
University of Texas MD Anderson Cancer Center
UT Medical Branch at Galveston
Mahidol University
Dankook University
Baylor College of Medicine
Kyung Hee University
miRcore
Keywords: Biochemistry, Genetics and Molecular Biology;Chemistry;Physics and Astronomy
Issue Date: 1-Dec-2018
Citation: Nature Communications. Vol.9, No.1 (2018)
Abstract: © 2018 The Author(s). Transforming growth factor-β (TGF-β) signaling and microRNAs (miRNAs) are important gene regulatory components in cancer. Usually in advanced malignant stages, TGF-β signaling is elevated but global miRNA expression is suppressed. Such a gene expression signature is well illustrated in a fibrosis (or mesenchymal) subtype of ovarian cancer (OC) that is of poor prognosis. However, the interplay between the two pathways in the OC subtype has not yet been elucidated. nc886 is a recently identified non-coding RNA implicated in several malignancies. The high expression of nc886 is associated with poor prognosis in 285 OC patients. Herein, we find that in OC nc886 expression is induced by TGF-β and that nc886 binds to Dicer to inhibit miRNA maturation. By preventing the miRNA pathway, nc886 emulates TGF-β in gene expression patterns and potentiates cell adhesion, migration, invasion, and drug resistance. Here we report nc886 to be a molecular link between the TGF-β and miRNA pathways.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85044445403&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/44985
ISSN: 20411723
Appears in Collections:Scopus 2018

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