Long non-coding RNA MANCR is a target of BET bromodomain protein BRD4 and plays a critical role in cellular migration and invasion abilities of prostate cancer.


Journal

Biochemical and biophysical research communications
ISSN: 1090-2104
Titre abrégé: Biochem Biophys Res Commun
Pays: United States
ID NLM: 0372516

Informations de publication

Date de publication:
21 05 2020
Historique:
received: 22 02 2020
accepted: 09 03 2020
pubmed: 23 3 2020
medline: 25 11 2020
entrez: 23 3 2020
Statut: ppublish

Résumé

Androgen receptor (AR)-negative castration-resistant prostate cancer (CRPC) is highly aggressive and is resistant to most of the current therapies. Bromodomain and extra terminal domain (BET) protein BRD4 binds to super-enhancers (SEs) that drive high expression of oncogenes in many cancers. A BET inhibitor, JQ1, has been found to suppress the malignant phenotypes of prostate cancer cells, however, the target genes of JQ1 remain largely unknown. Here we show that SE-associated genes specific for AR-negative CRPC PC3 cells include genes involved in migration and invasion, and that JQ1 impairs migration and invasion of PC3 cells. We identified a long non-coding RNA, MANCR, which was markedly down-regulated by JQ1, and found that BRD4 binds to the MANCR locus. MANCR knockdown led to a significant decrease in migration and invasion of PC3 cells. Furthermore, RNA sequencing analysis revealed that expression of the genes involved in migration and invasion was altered by MANCR knockdown. In summary, our data demonstrate that MANCR plays a critical role in migration and invasion of PC3 cells.

Identifiants

pubmed: 32199616
pii: S0006-291X(20)30522-2
doi: 10.1016/j.bbrc.2020.03.043
pii:
doi:

Substances chimiques

(+)-JQ1 compound 0
Azepines 0
BRD4 protein, human 0
Cell Cycle Proteins 0
RNA, Untranslated 0
Transcription Factors 0
Triazoles 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

128-134

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Masayuki Nagasawa (M)

Department of Biochemistry and Molecular Biology, Shiga University of Medical Science, Shiga, Japan; Department of Urology, Shiga University of Medical Science, Shiga, Japan.

Kosuke Tomimatsu (K)

Department of Biochemistry and Molecular Biology, Shiga University of Medical Science, Shiga, Japan.

Koji Terada (K)

Department of Biochemistry and Molecular Biology, Shiga University of Medical Science, Shiga, Japan.

Kenta Kondo (K)

Department of Biochemistry and Molecular Biology, Shiga University of Medical Science, Shiga, Japan.

Kazuko Miyazaki (K)

Laboratory of Immunology, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, Japan.

Masaki Miyazaki (M)

Laboratory of Immunology, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, Japan.

Daisuke Motooka (D)

Genome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.

Daisuke Okuzaki (D)

Genome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.

Tetsuya Yoshida (T)

Department of Urology, Shiga University of Medical Science, Shiga, Japan.

Susumu Kageyama (S)

Department of Urology, Shiga University of Medical Science, Shiga, Japan.

Hiroshi Kawamoto (H)

Laboratory of Immunology, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, Japan.

Akihiro Kawauchi (A)

Department of Urology, Shiga University of Medical Science, Shiga, Japan.

Yasutoshi Agata (Y)

Department of Biochemistry and Molecular Biology, Shiga University of Medical Science, Shiga, Japan. Electronic address: yagata@belle.shiga-med.ac.jp.

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Classifications MeSH