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CLK2 blockade modulates alternative splicing compromising MYC‐driven breast tumors

CLK2 blockade modulates alternative splicing compromising MYC‐driven breast tumors MYC oncogene overexpression/amplification is common in multiple human cancers, in which it regulates proliferation, apoptosis and cell metabolism, among other processes, and its expression associates with poor prognosis. Targeting MYC presents an exciting therapeutic possibility, but developing appropriate drugs that impair protein function remains challenging. Searching for alternative therapeutic options for treating aggressive MYC‐driven cancers is thus of high clinical interest. Intriguingly, MYC‐driven cancers present vulnerability against spliceosome inhibition. In this issue of EMBO Molecular Medicine, Iwai et al () tackle targeting the splicing regulatory Cdc2‐like kinase (CLKs) family. They report that a novel, orally administered CLK2 inhibitor (T‐025) induces exon skipping, which results in cancer cell growth reduction, especially in breast cancer (BCa) MYC‐driven tumors. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Embo Molecular Medicine Wiley

CLK2 blockade modulates alternative splicing compromising MYC‐driven breast tumors

Embo Molecular Medicine , Volume 10 (6) – Jan 1, 2018

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Publisher
Wiley
Copyright
© 2018 EMBO
ISSN
1757-4676
eISSN
1757-4684
DOI
10.15252/emmm.201809213
Publisher site
See Article on Publisher Site

Abstract

MYC oncogene overexpression/amplification is common in multiple human cancers, in which it regulates proliferation, apoptosis and cell metabolism, among other processes, and its expression associates with poor prognosis. Targeting MYC presents an exciting therapeutic possibility, but developing appropriate drugs that impair protein function remains challenging. Searching for alternative therapeutic options for treating aggressive MYC‐driven cancers is thus of high clinical interest. Intriguingly, MYC‐driven cancers present vulnerability against spliceosome inhibition. In this issue of EMBO Molecular Medicine, Iwai et al () tackle targeting the splicing regulatory Cdc2‐like kinase (CLKs) family. They report that a novel, orally administered CLK2 inhibitor (T‐025) induces exon skipping, which results in cancer cell growth reduction, especially in breast cancer (BCa) MYC‐driven tumors.

Journal

Embo Molecular MedicineWiley

Published: Jan 1, 2018

References