Commentary 10.1172/JCI96497

Epigenetics at the base of alternative splicing changes that promote colorectal cancer

Alberto R. Kornblihtt

Universidad de Buenos Aires (UBA), Facultad de Ciencias Exactas y Naturales, Departamento de Fisiología, Biología Molecular y Celular and CONICET-UBA, Instituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE), Buenos Aires, Argentina.

Address correspondence to: Alberto R. Kornblihtt, Ciudad Universitaria, Pabellón IFIBYNE. (1428) Buenos Aires, Argentina. Phone: 54.11.45763386; Email: ark@fbmc.fcen.uba.ar.

Find articles by Kornblihtt, A. in: JCI | PubMed | Google Scholar

First published August 21, 2017 - More info

Published in Volume 127, Issue 9 (September 1, 2017)
J Clin Invest. 2017;127(9):3281–3283. doi:10.1172/JCI96497.
Copyright © 2017, American Society for Clinical Investigation

First published August 21, 2017

See the related article at Histone methyltransferase SETD2 modulates alternative splicing to inhibit intestinal tumorigenesis.

Chromatin modification influences gene expression by either repressing or activating genes, depending on the specific histone mark. Chromatin structure can also influence alternative splicing of transcripts; however, the mechanisms by which epigenetic marks influence splicing are poorly understood. A report in the current issue of the JCI highlights the biological importance of the coordinated control of alternative pre-mRNA splicing by chromatin structure and transcriptional elongation. Yuan et al. found that mutation of the histone methyl transferase SEDT2 affects alternative splicing fates of several key regulatory genes, including those involved in Wnt signaling. As a consequence, loss of SEDT2 in the intestine aggravated Wnt/β-catenin signaling effects, thereby leading to colorectal cancer.

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