Epigenetic alterations of BRG1 leads to cancer development through its nuclear-cytoplasmic shuttling abnormalities

Esra Gunduz, Mehmet Gunduz, Hitoshi Nagatsuka, Levent Beder, Kadir Demircan, Ryo Tamamura, Omer Faruk Hatipoglu, Naila Mahmut, Naoki Katase, Yoshio Naomoto, Noriyuki Nagai

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)


SWI/SNF is a multiprotein chromatin remodeling complex important for gene regulation. BRG1 and its close relative BRM, have ATPase activity necessary for transcriptional regulation by conformational change of nucleosomes. Due to this role on gene expression, several members of SWI/SNF complex including BRG1 and BRM function as a tumor suppressor or negative regulator of cellular proliferation. On the other hand, the shuttling of proteins between nucleus and cytoplasm is strongly involved in the regulation of cell cycle and proliferation. Many of tumor suppressor gene (TSG)s including p53, BRCA1, ING1 play some of their functions through nucleocytoplasmic shuttling. Abnormalities related with this process abrogate the subcellular localization of the TSGs and lead to cancer development. We recently demonstrated BRG1 as a TSG in oral cancer. Our analysis also revealed an interesting finding that one of the splicing forms of BRG1 is selectively lost in cancer tissue as compared to normal counterparts. Our further analysis revealed a putative nuclear retention signal domain for this splicing form. In this article, we speculate the possible mechanism for the inactivation of BRG1 gene in oral cancer through an abnormality in its subcellular localization.

Original languageEnglish
Pages (from-to)1313-1316
Number of pages4
JournalMedical Hypotheses
Issue number6
Publication statusPublished - 2006

ASJC Scopus subject areas

  • General Medicine


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