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...
| Main Authors: | , , , , , |
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| Format: | Proceeding Paper |
| Language: | English English |
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2013
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| Online Access: | 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 |
| _version_ | 1848781272408653824 |
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| 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 |
| building | IIUM Repository |
| collection | Online Access |
| 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. |
| first_indexed | 2025-11-14T15:46:56Z |
| format | Proceeding Paper |
| id | iium-36682 |
| institution | International Islamic University Malaysia |
| institution_category | Local University |
| language | English English |
| last_indexed | 2025-11-14T15:46:56Z |
| publishDate | 2013 |
| recordtype | eprints |
| repository_type | Digital Repository |
| 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 Proceeding Paper 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 |
| 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 |
| title | 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_short | ARID3B silencing inhibits E2F-mediated transcription and cell proliferation |
| title_sort | arid3b silencing inhibits e2f-mediated transcription and cell proliferation |
| topic | RK Dentistry |
| 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 |