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Inhibition of transforming growth factor beta/SMAD signal by MiR-155 is involved in arsenic trioxide-induced anti-angiogenesis in prostate cancer

Prostate cancer is the most common cause of cancer-related deaths in men. Current practices for treatment of prostate cancer are less than satisfactory because of metastasis and recurrence, which are primarily attributed to angiogenesis. Hence, anti-angiogenesis treatment is becoming a promising new...

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Autores principales: Ji, Hui, Li, Yuan, Jiang, Fei, Wang, Xingxing, Zhang, Jianping, Shen, Jian, Yang, Xiaojun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4317958/
https://www.ncbi.nlm.nih.gov/pubmed/25283513
http://dx.doi.org/10.1111/cas.12548
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author Ji, Hui
Li, Yuan
Jiang, Fei
Wang, Xingxing
Zhang, Jianping
Shen, Jian
Yang, Xiaojun
author_facet Ji, Hui
Li, Yuan
Jiang, Fei
Wang, Xingxing
Zhang, Jianping
Shen, Jian
Yang, Xiaojun
author_sort Ji, Hui
collection PubMed
description Prostate cancer is the most common cause of cancer-related deaths in men. Current practices for treatment of prostate cancer are less than satisfactory because of metastasis and recurrence, which are primarily attributed to angiogenesis. Hence, anti-angiogenesis treatment is becoming a promising new approach for prostate cancer therapy. In addition to treating acute promyelocytic leukemia, arsenic trioxide (As(2)O(3)) suppresses other solid tumors, including prostate cancer. However, the effects of As(2)O(3) on angiogenesis in prostate cancer cells, and the underlying molecular mechanisms remain unclear. In the present study, As(2)O(3) attenuated angiogenic ability through microRNA-155 (miR-155)-mediated inhibition of transforming growth factor beta (TGF-β)/SMAD signal pathway in human prostate cancer PC-3 and LNCaP cells in vitro and in vivo. Briefly, As(2)O(3) inhibited the activations/expressions of both TGFβ-induced and endogenous SMAD2/3. Furthermore, As(2)O(3) improved the expression of miR-155 via DNA-demethylation. MiR-155, which targeted the SMAD2-3′UTR, decreased the expression and function of SMAD2. Knockdown of miR-155 abolished the As(2)O(3)-induced inhibitions of the TGF-β/SMAD2 signaling, the vascular endothelial growth factor secretion and angiogenesis. Through understanding a novel mechanism whereby As(2)O(3) inhibits angiogenic potential of prostate cancer cells, our study would help in the development of As(2)O(3) as a potential chemopreventive agent when used alone or in combination with other current anticancer drugs.
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spelling pubmed-43179582015-10-05 Inhibition of transforming growth factor beta/SMAD signal by MiR-155 is involved in arsenic trioxide-induced anti-angiogenesis in prostate cancer Ji, Hui Li, Yuan Jiang, Fei Wang, Xingxing Zhang, Jianping Shen, Jian Yang, Xiaojun Cancer Sci Original Articles Prostate cancer is the most common cause of cancer-related deaths in men. Current practices for treatment of prostate cancer are less than satisfactory because of metastasis and recurrence, which are primarily attributed to angiogenesis. Hence, anti-angiogenesis treatment is becoming a promising new approach for prostate cancer therapy. In addition to treating acute promyelocytic leukemia, arsenic trioxide (As(2)O(3)) suppresses other solid tumors, including prostate cancer. However, the effects of As(2)O(3) on angiogenesis in prostate cancer cells, and the underlying molecular mechanisms remain unclear. In the present study, As(2)O(3) attenuated angiogenic ability through microRNA-155 (miR-155)-mediated inhibition of transforming growth factor beta (TGF-β)/SMAD signal pathway in human prostate cancer PC-3 and LNCaP cells in vitro and in vivo. Briefly, As(2)O(3) inhibited the activations/expressions of both TGFβ-induced and endogenous SMAD2/3. Furthermore, As(2)O(3) improved the expression of miR-155 via DNA-demethylation. MiR-155, which targeted the SMAD2-3′UTR, decreased the expression and function of SMAD2. Knockdown of miR-155 abolished the As(2)O(3)-induced inhibitions of the TGF-β/SMAD2 signaling, the vascular endothelial growth factor secretion and angiogenesis. Through understanding a novel mechanism whereby As(2)O(3) inhibits angiogenic potential of prostate cancer cells, our study would help in the development of As(2)O(3) as a potential chemopreventive agent when used alone or in combination with other current anticancer drugs. Blackwell Publishing Ltd 2014-12 2014-11-05 /pmc/articles/PMC4317958/ /pubmed/25283513 http://dx.doi.org/10.1111/cas.12548 Text en © 2014 The Authors. Cancer Science published by Wiley Publishing Asia Pty Ltd on behalf of Japanese Cancer Association. http://creativecommons.org/licenses/by-nc-nd/3.0/ This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Original Articles
Ji, Hui
Li, Yuan
Jiang, Fei
Wang, Xingxing
Zhang, Jianping
Shen, Jian
Yang, Xiaojun
Inhibition of transforming growth factor beta/SMAD signal by MiR-155 is involved in arsenic trioxide-induced anti-angiogenesis in prostate cancer
title Inhibition of transforming growth factor beta/SMAD signal by MiR-155 is involved in arsenic trioxide-induced anti-angiogenesis in prostate cancer
title_full Inhibition of transforming growth factor beta/SMAD signal by MiR-155 is involved in arsenic trioxide-induced anti-angiogenesis in prostate cancer
title_fullStr Inhibition of transforming growth factor beta/SMAD signal by MiR-155 is involved in arsenic trioxide-induced anti-angiogenesis in prostate cancer
title_full_unstemmed Inhibition of transforming growth factor beta/SMAD signal by MiR-155 is involved in arsenic trioxide-induced anti-angiogenesis in prostate cancer
title_short Inhibition of transforming growth factor beta/SMAD signal by MiR-155 is involved in arsenic trioxide-induced anti-angiogenesis in prostate cancer
title_sort inhibition of transforming growth factor beta/smad signal by mir-155 is involved in arsenic trioxide-induced anti-angiogenesis in prostate cancer
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4317958/
https://www.ncbi.nlm.nih.gov/pubmed/25283513
http://dx.doi.org/10.1111/cas.12548
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