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Basic helix-loop-helix transcription factor DEC2 functions as an anti-apoptotic factor during paclitaxel-induced apoptosis in human prostate cancer cells

The functions of basic helix-loop-helix (bHLH) transcription factor-differentiated embryonic chondrocyte (DEC)1 (BHLHE40) and 2 (BHLHE41) are involved in various fields such as circadian rhythms, immune responses, cell proliferation, hypoxia reaction as well as malignant tumors. Previous findings sh...

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Autores principales: Liu, Qiang, Wu, Yunyan, Yoshizawa, Tadashi, Yan, Xu, Morohashi, Satoko, Seino, Hiroko, Kato, Yukio, Kijima, Hiroshi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5117753/
https://www.ncbi.nlm.nih.gov/pubmed/27840924
http://dx.doi.org/10.3892/ijmm.2016.2798
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author Liu, Qiang
Wu, Yunyan
Yoshizawa, Tadashi
Yan, Xu
Morohashi, Satoko
Seino, Hiroko
Kato, Yukio
Kijima, Hiroshi
author_facet Liu, Qiang
Wu, Yunyan
Yoshizawa, Tadashi
Yan, Xu
Morohashi, Satoko
Seino, Hiroko
Kato, Yukio
Kijima, Hiroshi
author_sort Liu, Qiang
collection PubMed
description The functions of basic helix-loop-helix (bHLH) transcription factor-differentiated embryonic chondrocyte (DEC)1 (BHLHE40) and 2 (BHLHE41) are involved in various fields such as circadian rhythms, immune responses, cell proliferation, hypoxia reaction as well as malignant tumors. Previous findings showed that DEC served as apoptosis regulators of various cancer cell lines. However, little is known regarding the expression of DEC1 and DEC2 in prostate cancer cells. The present study aimed to examine the roles of DEC1 and DEC2 in human prostate cancer DU145 and PC-3 cells that were treated with paclitaxel. The expression of DEC1 and DEC2 was decreased in DU145 cells but was increased in PC-3 cells when treated with paclitaxel. DU145 cells were more sensitive to paclitaxel than PC-3 cells since the amount of cleaved poly(ADP-ribose) polymerase (PARP) reached its peak at 50 μM of paclitaxel in DU145 cells but at 100 μM in PC-3 cells. In addition, the amount of cleaved PARP was decreased by DEC1 siRNA, while it was increased by DEC2 siRNA in the presence of paclitaxel. Although DEC2 overexpression slightly inhibited cleaved PARP in the two cell lines, the effects of DEC1 overexpression on apoptosis remain to be determined. In conclusion, DEC1, at least partly, exerted a pro-apoptotic effect, whereas DEC2 exerted an anti-apoptotic effect in paclitaxel-induced apoptosis of human prostate cancer cells.
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spelling pubmed-51177532016-11-28 Basic helix-loop-helix transcription factor DEC2 functions as an anti-apoptotic factor during paclitaxel-induced apoptosis in human prostate cancer cells Liu, Qiang Wu, Yunyan Yoshizawa, Tadashi Yan, Xu Morohashi, Satoko Seino, Hiroko Kato, Yukio Kijima, Hiroshi Int J Mol Med Articles The functions of basic helix-loop-helix (bHLH) transcription factor-differentiated embryonic chondrocyte (DEC)1 (BHLHE40) and 2 (BHLHE41) are involved in various fields such as circadian rhythms, immune responses, cell proliferation, hypoxia reaction as well as malignant tumors. Previous findings showed that DEC served as apoptosis regulators of various cancer cell lines. However, little is known regarding the expression of DEC1 and DEC2 in prostate cancer cells. The present study aimed to examine the roles of DEC1 and DEC2 in human prostate cancer DU145 and PC-3 cells that were treated with paclitaxel. The expression of DEC1 and DEC2 was decreased in DU145 cells but was increased in PC-3 cells when treated with paclitaxel. DU145 cells were more sensitive to paclitaxel than PC-3 cells since the amount of cleaved poly(ADP-ribose) polymerase (PARP) reached its peak at 50 μM of paclitaxel in DU145 cells but at 100 μM in PC-3 cells. In addition, the amount of cleaved PARP was decreased by DEC1 siRNA, while it was increased by DEC2 siRNA in the presence of paclitaxel. Although DEC2 overexpression slightly inhibited cleaved PARP in the two cell lines, the effects of DEC1 overexpression on apoptosis remain to be determined. In conclusion, DEC1, at least partly, exerted a pro-apoptotic effect, whereas DEC2 exerted an anti-apoptotic effect in paclitaxel-induced apoptosis of human prostate cancer cells. D.A. Spandidos 2016-12 2016-11-08 /pmc/articles/PMC5117753/ /pubmed/27840924 http://dx.doi.org/10.3892/ijmm.2016.2798 Text en Copyright: © Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , 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 Articles
Liu, Qiang
Wu, Yunyan
Yoshizawa, Tadashi
Yan, Xu
Morohashi, Satoko
Seino, Hiroko
Kato, Yukio
Kijima, Hiroshi
Basic helix-loop-helix transcription factor DEC2 functions as an anti-apoptotic factor during paclitaxel-induced apoptosis in human prostate cancer cells
title Basic helix-loop-helix transcription factor DEC2 functions as an anti-apoptotic factor during paclitaxel-induced apoptosis in human prostate cancer cells
title_full Basic helix-loop-helix transcription factor DEC2 functions as an anti-apoptotic factor during paclitaxel-induced apoptosis in human prostate cancer cells
title_fullStr Basic helix-loop-helix transcription factor DEC2 functions as an anti-apoptotic factor during paclitaxel-induced apoptosis in human prostate cancer cells
title_full_unstemmed Basic helix-loop-helix transcription factor DEC2 functions as an anti-apoptotic factor during paclitaxel-induced apoptosis in human prostate cancer cells
title_short Basic helix-loop-helix transcription factor DEC2 functions as an anti-apoptotic factor during paclitaxel-induced apoptosis in human prostate cancer cells
title_sort basic helix-loop-helix transcription factor dec2 functions as an anti-apoptotic factor during paclitaxel-induced apoptosis in human prostate cancer cells
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5117753/
https://www.ncbi.nlm.nih.gov/pubmed/27840924
http://dx.doi.org/10.3892/ijmm.2016.2798
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