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miR-489-3p inhibits proliferation and migration of bladder cancer cells through downregulation of histone deacetylase 2

Since human bladder cancer (BC) is a common malignancy of the urinary system with poor prognosis, it is crucial to clarify the molecular mechanisms of BC development and progression. To the best of our knowledge, the current study demonstrated for the first time that miR-489-3p suppressed BC cell-de...

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Autores principales: Sun, Dan, Li, Tianren, Xin, Haotian, An, Jun, Yang, Jieping, Lin, Jiaxing, Meng, Xin, Wang, Biao, Ozaki, Toshinori, Yu, Meng, Zhu, Yuyan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7405606/
https://www.ncbi.nlm.nih.gov/pubmed/32774482
http://dx.doi.org/10.3892/ol.2020.11869
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author Sun, Dan
Li, Tianren
Xin, Haotian
An, Jun
Yang, Jieping
Lin, Jiaxing
Meng, Xin
Wang, Biao
Ozaki, Toshinori
Yu, Meng
Zhu, Yuyan
author_facet Sun, Dan
Li, Tianren
Xin, Haotian
An, Jun
Yang, Jieping
Lin, Jiaxing
Meng, Xin
Wang, Biao
Ozaki, Toshinori
Yu, Meng
Zhu, Yuyan
author_sort Sun, Dan
collection PubMed
description Since human bladder cancer (BC) is a common malignancy of the urinary system with poor prognosis, it is crucial to clarify the molecular mechanisms of BC development and progression. To the best of our knowledge, the current study demonstrated for the first time that miR-489-3p suppressed BC cell-derived tumor growth in vivo via the downregulation of histone deacetylase 2 (HDAC2). According to the results, expression levels of miR-489-3p were lower in BC tissues compared with corresponding normal tissues. Expression of miR-489-3p mimics in BC-derived T24 and 5637 cells resulted in a significant reduction in proliferation and migration rates. Furthermore, bioinformatics analyses indicated that HDAC2 may be a potential downstream target of miR-489-3p. In contrast to miR-489-3p, HDAC2 was expressed at higher levels in BC tissues compared with corresponding normal tissues. Additionally, small interfering RNA-mediated knockdown of HDAC2 caused a marked decrease in the proliferation and migration rates of T24 and 5637 cells. Consistent with these observations, expression of miR-489-3p mimics attenuated the growth of xenograft tumors arising from T24 cells and resulted in HDAC2 downregulation. In conclusion, the results of the current study indicated that the miR-489-3p/HDAC2 axis serves a role in the development and/or the progression of BC and may be a potential molecular target for the development of a novel strategy to treat patients with BC.
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spelling pubmed-74056062020-08-06 miR-489-3p inhibits proliferation and migration of bladder cancer cells through downregulation of histone deacetylase 2 Sun, Dan Li, Tianren Xin, Haotian An, Jun Yang, Jieping Lin, Jiaxing Meng, Xin Wang, Biao Ozaki, Toshinori Yu, Meng Zhu, Yuyan Oncol Lett Articles Since human bladder cancer (BC) is a common malignancy of the urinary system with poor prognosis, it is crucial to clarify the molecular mechanisms of BC development and progression. To the best of our knowledge, the current study demonstrated for the first time that miR-489-3p suppressed BC cell-derived tumor growth in vivo via the downregulation of histone deacetylase 2 (HDAC2). According to the results, expression levels of miR-489-3p were lower in BC tissues compared with corresponding normal tissues. Expression of miR-489-3p mimics in BC-derived T24 and 5637 cells resulted in a significant reduction in proliferation and migration rates. Furthermore, bioinformatics analyses indicated that HDAC2 may be a potential downstream target of miR-489-3p. In contrast to miR-489-3p, HDAC2 was expressed at higher levels in BC tissues compared with corresponding normal tissues. Additionally, small interfering RNA-mediated knockdown of HDAC2 caused a marked decrease in the proliferation and migration rates of T24 and 5637 cells. Consistent with these observations, expression of miR-489-3p mimics attenuated the growth of xenograft tumors arising from T24 cells and resulted in HDAC2 downregulation. In conclusion, the results of the current study indicated that the miR-489-3p/HDAC2 axis serves a role in the development and/or the progression of BC and may be a potential molecular target for the development of a novel strategy to treat patients with BC. D.A. Spandidos 2020-10 2020-07-15 /pmc/articles/PMC7405606/ /pubmed/32774482 http://dx.doi.org/10.3892/ol.2020.11869 Text en Copyright: © Sun et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ) and either DOI or URL of the article must be cited.
spellingShingle Articles
Sun, Dan
Li, Tianren
Xin, Haotian
An, Jun
Yang, Jieping
Lin, Jiaxing
Meng, Xin
Wang, Biao
Ozaki, Toshinori
Yu, Meng
Zhu, Yuyan
miR-489-3p inhibits proliferation and migration of bladder cancer cells through downregulation of histone deacetylase 2
title miR-489-3p inhibits proliferation and migration of bladder cancer cells through downregulation of histone deacetylase 2
title_full miR-489-3p inhibits proliferation and migration of bladder cancer cells through downregulation of histone deacetylase 2
title_fullStr miR-489-3p inhibits proliferation and migration of bladder cancer cells through downregulation of histone deacetylase 2
title_full_unstemmed miR-489-3p inhibits proliferation and migration of bladder cancer cells through downregulation of histone deacetylase 2
title_short miR-489-3p inhibits proliferation and migration of bladder cancer cells through downregulation of histone deacetylase 2
title_sort mir-489-3p inhibits proliferation and migration of bladder cancer cells through downregulation of histone deacetylase 2
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7405606/
https://www.ncbi.nlm.nih.gov/pubmed/32774482
http://dx.doi.org/10.3892/ol.2020.11869
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