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
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 i...
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| Published in | Biochemical and biophysical research communications Vol. 526; no. 1; pp. 128 - 134 |
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| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
21.05.2020
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0006-291X 1090-2104 1090-2104 |
| DOI | 10.1016/j.bbrc.2020.03.043 |
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| Abstract | 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.
•Super-enhancer associated genes in PC3 cells are enriched in EMT pathways.•Migratory and invasive abilities of PC3 cells are reduced by BET protein inhibitor.•The lncRNA MANCR is markedly down-regulated by BET protein inhibitor in PC3 cells.•MANCR positively regulates cell migration and invasion in prostate cancer cell lines. |
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| AbstractList | 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. 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. •Super-enhancer associated genes in PC3 cells are enriched in EMT pathways.•Migratory and invasive abilities of PC3 cells are reduced by BET protein inhibitor.•The lncRNA MANCR is markedly down-regulated by BET protein inhibitor in PC3 cells.•MANCR positively regulates cell migration and invasion in prostate cancer cell lines. 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.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. |
| Author | Kawauchi, Akihiro Terada, Koji Miyazaki, Kazuko Nagasawa, Masayuki Miyazaki, Masaki Kondo, Kenta Kawamoto, Hiroshi Kageyama, Susumu Okuzaki, Daisuke Tomimatsu, Kosuke Motooka, Daisuke Yoshida, Tetsuya Agata, Yasutoshi |
| Author_xml | – sequence: 1 givenname: Masayuki orcidid: 0000-0003-1299-6354 surname: Nagasawa fullname: Nagasawa, Masayuki organization: Department of Biochemistry and Molecular Biology, Shiga University of Medical Science, Shiga, Japan – sequence: 2 givenname: Kosuke orcidid: 0000-0003-3733-6686 surname: Tomimatsu fullname: Tomimatsu, Kosuke organization: Department of Biochemistry and Molecular Biology, Shiga University of Medical Science, Shiga, Japan – sequence: 3 givenname: Koji surname: Terada fullname: Terada, Koji organization: Department of Biochemistry and Molecular Biology, Shiga University of Medical Science, Shiga, Japan – sequence: 4 givenname: Kenta surname: Kondo fullname: Kondo, Kenta organization: Department of Biochemistry and Molecular Biology, Shiga University of Medical Science, Shiga, Japan – sequence: 5 givenname: Kazuko surname: Miyazaki fullname: Miyazaki, Kazuko organization: Laboratory of Immunology, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, Japan – sequence: 6 givenname: Masaki surname: Miyazaki fullname: Miyazaki, Masaki organization: Laboratory of Immunology, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, Japan – sequence: 7 givenname: Daisuke surname: Motooka fullname: Motooka, Daisuke organization: Genome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan – sequence: 8 givenname: Daisuke surname: Okuzaki fullname: Okuzaki, Daisuke organization: Genome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan – sequence: 9 givenname: Tetsuya orcidid: 0000-0002-4520-3640 surname: Yoshida fullname: Yoshida, Tetsuya organization: Department of Urology, Shiga University of Medical Science, Shiga, Japan – sequence: 10 givenname: Susumu orcidid: 0000-0001-7150-647X surname: Kageyama fullname: Kageyama, Susumu organization: Department of Urology, Shiga University of Medical Science, Shiga, Japan – sequence: 11 givenname: Hiroshi surname: Kawamoto fullname: Kawamoto, Hiroshi organization: Laboratory of Immunology, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, Japan – sequence: 12 givenname: Akihiro surname: Kawauchi fullname: Kawauchi, Akihiro organization: Department of Urology, Shiga University of Medical Science, Shiga, Japan – sequence: 13 givenname: Yasutoshi surname: Agata fullname: Agata, Yasutoshi email: yagata@belle.shiga-med.ac.jp organization: Department of Biochemistry and Molecular Biology, Shiga University of Medical Science, Shiga, Japan |
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| Keywords | Epithelial-mesenchymal transition Super-enhancer MANCR lncRNA BET protein inhibitor Prostate cancer |
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| SubjectTerms | androgen receptors BET protein inhibitor cell movement Epithelial-mesenchymal transition lncRNA loci MANCR non-coding RNA oncogenes Prostate cancer prostatic neoplasms Super-enhancer |
| Title | 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 |
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