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ARID3B silencing inhibits E2F-mediated transcription and cell proliferation

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 (Unpublished)

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Abstract

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.

Item Type: Conference or Workshop Item (Abstract)
Additional Information: 6863/36682
Uncontrolled Keywords: ARID3B silencing
Subjects: R Medicine > RK Dentistry
Kulliyyahs/Centres/Divisions/Institutes: Kulliyyah of Dentistry
Depositing User: Dr Widya Lestari
Date Deposited: 22 Mar 2016 10:17
Last Modified: 22 Mar 2016 10:17
URI: http://irep.iium.edu.my/id/eprint/36682

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