ARID3B silencing inhibits E2F-mediated transcription and cell proliferation

ARID3B is a member of ARID3 (AT-rich interacting domain) family of DNA-binding proteins, and overexpressed in human malignant tumors. The closely related family member, ARID3A, was isolated as a protein binding to E2F1 transcription factor and activates E2F-dependent transcription. However, the func...

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Main Authors:	A. S. M. Saadat, Khandakar, Lestari, Widya, Teng, Ma, Pratama, Endrawan, Ohtani, Kiyoshi, Ikeda, Masa-Aki
Format:	Conference or Workshop Item
Language:	English English
Published:	2013
Subjects:	RK Dentistry
Online Access:	http://irep.iium.edu.my/36682/ http://irep.iium.edu.my/36682/ http://irep.iium.edu.my/36682/1/widaya.pdf http://irep.iium.edu.my/36682/4/The_36th_Annual_Meeting_of_the_Molecular_Biology_Society_of_Japan.pdf

id	iium-36682
recordtype	eprints
spelling	iium-366822016-03-22T02:17:19Z http://irep.iium.edu.my/36682/ ARID3B silencing inhibits E2F-mediated transcription and cell proliferation A. S. M. Saadat, Khandakar Lestari, Widya Teng, Ma Pratama, Endrawan Ohtani, Kiyoshi Ikeda, Masa-Aki RK Dentistry ARID3B is a member of ARID3 (AT-rich interacting domain) family of DNA-binding proteins, and overexpressed in human malignant tumors. The closely related family member, ARID3A, was isolated as a protein binding to E2F1 transcription factor and activates E2F-dependent transcription. However, the function of ARID3B in the regulation of E2F-responsive genes remains largely unknown. Here, we show that siRNA-mediated gene silncing of ARID3B blocked transcription of E2F-responsive genes, such as E2F1,p107,cyclin E1, CDC2 and CDC6 in normal human dermal fibroblast (NHDFs). Ectopic overexpression of ARID3B up-regulated transcription of these E2F-responsive genes in quisencet NHDFs. Furthermore, the inhibition of cyclin E1 expression by ARId3B silencing was not restored by E2F1. We found putative ARID3-binding sites in the E2F-responsive genes and show that ARID3A and ARID3B were recruited to these sites in vivo. Mutation of putative ARID3-binding sites reduced the CDC promoter activity in both serum-starved and stimulated conditions. Finally, ARID3B silencing attenuated S phase entry of NHDFs, and suppressed tumor cell growth. These results indicate that ARID3B play an important role for E2F-meditaed transcriptional activation and cell proliferation. 2013 Conference or Workshop Item NonPeerReviewed application/pdf en http://irep.iium.edu.my/36682/1/widaya.pdf application/pdf en http://irep.iium.edu.my/36682/4/The_36th_Annual_Meeting_of_the_Molecular_Biology_Society_of_Japan.pdf A. S. M. Saadat, Khandakar and Lestari, Widya and Teng, Ma and Pratama, Endrawan and Ohtani, Kiyoshi and Ikeda, Masa-Aki (2013) ARID3B silencing inhibits E2F-mediated transcription and cell proliferation. In: The 36th Annual Meeting of the Molecular Biology Society of Japan 2013, 3rd-6th Dec. 2013, Kobe International Conference Centre, Japan. (Unpublished) http://www.mbsj.jp/meetings/annual/2013/program/24.poster.pdf
repository_type	Digital Repository
institution_category	Local University
institution	International Islamic University Malaysia
building	IIUM Repository
collection	Online Access
language	English English
topic	RK Dentistry
spellingShingle	RK Dentistry A. S. M. Saadat, Khandakar Lestari, Widya Teng, Ma Pratama, Endrawan Ohtani, Kiyoshi Ikeda, Masa-Aki ARID3B silencing inhibits E2F-mediated transcription and cell proliferation
description	ARID3B is a member of ARID3 (AT-rich interacting domain) family of DNA-binding proteins, and overexpressed in human malignant tumors. The closely related family member, ARID3A, was isolated as a protein binding to E2F1 transcription factor and activates E2F-dependent transcription. However, the function of ARID3B in the regulation of E2F-responsive genes remains largely unknown. Here, we show that siRNA-mediated gene silncing of ARID3B blocked transcription of E2F-responsive genes, such as E2F1,p107,cyclin E1, CDC2 and CDC6 in normal human dermal fibroblast (NHDFs). Ectopic overexpression of ARID3B up-regulated transcription of these E2F-responsive genes in quisencet NHDFs. Furthermore, the inhibition of cyclin E1 expression by ARId3B silencing was not restored by E2F1. We found putative ARID3-binding sites in the E2F-responsive genes and show that ARID3A and ARID3B were recruited to these sites in vivo. Mutation of putative ARID3-binding sites reduced the CDC promoter activity in both serum-starved and stimulated conditions. Finally, ARID3B silencing attenuated S phase entry of NHDFs, and suppressed tumor cell growth. These results indicate that ARID3B play an important role for E2F-meditaed transcriptional activation and cell proliferation.
format	Conference or Workshop Item
author	A. S. M. Saadat, Khandakar Lestari, Widya Teng, Ma Pratama, Endrawan Ohtani, Kiyoshi Ikeda, Masa-Aki
author_facet	A. S. M. Saadat, Khandakar Lestari, Widya Teng, Ma Pratama, Endrawan Ohtani, Kiyoshi Ikeda, Masa-Aki
author_sort	A. S. M. Saadat, Khandakar
title	ARID3B silencing inhibits E2F-mediated transcription and cell proliferation
title_short	ARID3B silencing inhibits E2F-mediated transcription and cell proliferation
title_full	ARID3B silencing inhibits E2F-mediated transcription and cell proliferation
title_fullStr	ARID3B silencing inhibits E2F-mediated transcription and cell proliferation
title_full_unstemmed	ARID3B silencing inhibits E2F-mediated transcription and cell proliferation
title_sort	arid3b silencing inhibits e2f-mediated transcription and cell proliferation
publishDate	2013
url	http://irep.iium.edu.my/36682/ http://irep.iium.edu.my/36682/ http://irep.iium.edu.my/36682/1/widaya.pdf http://irep.iium.edu.my/36682/4/The_36th_Annual_Meeting_of_the_Molecular_Biology_Society_of_Japan.pdf
first_indexed	2023-09-18T20:52:33Z
last_indexed	2023-09-18T20:52:33Z
_version_	1777410091491786752

ARID3B silencing inhibits E2F-mediated transcription and cell proliferation

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