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Regulation of DU145 prostate cancer cell growth by Scm-like with four mbt domains 2

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Abstract

Mammalian SFMBTs have been considered to be polycomb group repressors. However, molecular mechanisms underlying mammalian SFMBTs-mediated gene regulation and their biological function have not been characterized. In the present study, we identified YY1 and methylated histones as interacting proteins of human SFMBT2. We also found that human SFMBT2 binds preferentially to methylated histone H3 and H4 that are associated with transcriptional repression. Using DU145 prostate cancer cells as a model, we showed that SFMBT2 has a transcriptional repression activity on HOXB13 gene expression. In addition, occupancy of SFMBT2 coincided with enrichment of di- and tri-methylated H3K9 and H4K20 as well as tri-methylated H3K27 at the HOXB13 gene promoter. When SFMBT2 was depleted by siRNA in DU145 prostate cancer cells, significant up-regulation of HOXB13 gene expression and decreased cell growth were observed. Collectively, our findings indicate that human SFMBT2 may regulate cell growth via epigenetic regulation of HOXB13 gene expression in DU145 prostate cancer cells.

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Acknowledgements

No author on this manuscript reported any conflict of interest. This work was supported by Basic Science Research Program (20110003578) and National Nuclear R&DProgram (20100017607) through the National Research Foundation of Korea (NSF) funded by the Ministry of Education, Science and Technology, the Republic of Korea.

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Correspondence to Bong-Gun Ju.

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Corresponding editor: Indranil Dasgupta

MS received 02 August 2012; accepted 14 November 2012

Corresponding editor: Indranil Dasgupta

[Lee K, Na W , Maeng J-H, Wu H and Ju B-G 2013 Regulation of DU145 prostate cancer cell growth by Scm-like with four mbt domains 2. J. Biosci. 38 1–8] DOI 10.1007/s12038-012-9283-6

Kwanghyun Lee and Wonho Na contributed equally to this work.

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Lee, K., Na, W., Maeng, JH. et al. Regulation of DU145 prostate cancer cell growth by Scm-like with four mbt domains 2. J Biosci 38, 105–112 (2013). https://doi.org/10.1007/s12038-012-9283-6

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  • DOI: https://doi.org/10.1007/s12038-012-9283-6

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