Commentary 10.1172/JCI94763

A SMAP in the face for cancer

Shirish Shenolikar

Program in Cardiovascular and Metabolic Disorders, Duke-NUS Medical School Singapore, Singapore.

Address correspondence to: Shirish Shenolikar, Program in Cardiovascular and Metabolic Disorders, Duke-NUS Medical School Singapore, 8 College Road, Singapore 169857, Singapore. Phone: 65.6221.8625; E-mail: shirish.shenolikar@duke-NUS.edu.sg.

Find articles by Shenolikar, S. in: JCI | PubMed | Google Scholar

First published May 15, 2017 - More info

Published in Volume 127, Issue 6 (June 1, 2017)
J Clin Invest. 2017;127(6):2048–2050. doi:10.1172/JCI94763.
Copyright © 2017, American Society for Clinical Investigation

First published May 15, 2017

See the related article at Activation of tumor suppressor protein PP2A inhibits KRAS-driven tumor growth.

Observed deficits in protein phosphatase 2A (PP2A) function in a variety of human cancers have stimulated drug discovery efforts aimed at restoring PP2A function to inhibit tumor growth. Work published by Sangodkar et al. in this issue of the JCI describes the characterization of orally available small molecule activators of PP2A (SMAPs). These SMAPs attenuated mitogenic signaling and triggered apoptosis in KRAS-mutant lung cancer cells and inhibited tumor growth in murine models. Tumors with mutations in the SMAP-binding site of the PP2A A subunit displayed resistance to SMAPs. Future studies that identify the PP2A-regulated events targeted by SMAPs should guide critical decisions about which cancers might be best treated with these molecules. This study provides encouraging evidence in favor of SMAPs as potential anticancer drugs.

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