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Mathai J, Mittal SP, Alam A, et al. SMAR1 binds to T(C/G) repeat and inhibits tumor progression by regulating miR-371-373 cluster. Sci Rep. 2016;6:33779doi: 10.1038/srep33779.
Mathai, J., Mittal, S. P., Alam, A., Ranade, P., Mogare, D., Patel, S., Saxena, S., Ghorai, S., Kulkarni, A. P., & Chattopadhyay, S. (2016). SMAR1 binds to T(C/G) repeat and inhibits tumor progression by regulating miR-371-373 cluster. Scientific reports, 633779. https://doi.org/10.1038/srep33779
Mathai, Jinumary, et al. "SMAR1 binds to T(C/G) repeat and inhibits tumor progression by regulating miR-371-373 cluster." Scientific reports vol. 6 (2016): 33779. doi: https://doi.org/10.1038/srep33779
Mathai J, Mittal SP, Alam A, Ranade P, Mogare D, Patel S, Saxena S, Ghorai S, Kulkarni AP, Chattopadhyay S. SMAR1 binds to T(C/G) repeat and inhibits tumor progression by regulating miR-371-373 cluster. Sci Rep. 2016 Sep 27;6:33779. doi: 10.1038/srep33779. PMID: 27671416; PMCID: PMC5037395.
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Sci Rep. 2016 Sep 27;6:33779. doi: 10.1038/srep33779.

SMAR1 binds to T(C/G) repeat and inhibits tumor progression by regulating miR-371-373 cluster.

Scientific reports

Jinumary Mathai, Smriti P K Mittal, Aftab Alam, Payal Ranade, Devraj Mogare, Sonal Patel, Smita Saxena, Suvankar Ghorai, Abhijeet P Kulkarni, Samit Chattopadhyay

Affiliations

  1. Chromatin and Disease Biology Lab, National Centre for Cell Science, Savitribai Phule Pune University Campus, Ganeshkhind, Pune-411007, India.
  2. Department of Zoology, Savitribai Phule Pune University Campus, Pune 411007, India.
  3. Bioinformatics Centre, Savitribai Phule Pune University Campus, Pune 411007, India.

PMID: 27671416 PMCID: PMC5037395 DOI: 10.1038/srep33779

Abstract

Chromatin architecture and dynamics are regulated by various histone and non-histone proteins. The matrix attachment region binding proteins (MARBPs) play a central role in chromatin organization and function through numerous regulatory proteins. In the present study, we demonstrate that nuclear matrix protein SMAR1 orchestrates global gene regulation as determined by massively parallel ChIP-sequencing. The study revealed that SMAR1 binds to T(C/G) repeat and targets genes involved in diverse biological pathways. We observe that SMAR1 binds and targets distinctly different genes based on the availability of p53. Our data suggest that SMAR1 binds and regulates one of the imperative microRNA clusters in cancer and metastasis, miR-371-373. It negatively regulates miR-371-373 transcription as confirmed by SMAR1 overexpression and knockdown studies. Further, deletion studies indicate that a ~200 bp region in the miR-371-373 promoter is necessary for SMAR1 binding and transcriptional repression. Recruitment of HDAC1/mSin3A complex by SMAR1, concomitant with alteration of histone marks results in downregulation of the miRNA cluster. The regulation of miR-371-373 by SMAR1 inhibits breast cancer tumorigenesis and metastasis as determined by in vivo experiments. Overall, our study highlights the binding of SMAR1 to T(C/G) repeat and its role in cancer through miR-371-373.

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