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KSR1 and EPHB4 Regulate Myc and PGC1β To Promote Survival of Human Colon Tumors

KSR1 and EPHB4 Regulate Myc and PGC1β To Promote Survival of Human Colon Tumors

Jamie L McCall, Drew Gehring, Beth K Clymer, Kurt W Fisher, Binita Das, David L Kelly, Hyunseok Kim, Michael A White, Robert E Lewis

Mol Cell Biol. 2016 Aug 12;36(17):2246-61.

PMID: 27273865

Abstract:

Identification and characterization of survival pathways active in tumor cells but absent in normal tissues provide opportunities to develop effective anticancer therapies with reduced toxicity to the patient. We show here that, like kinase suppressor of Ras 1 (KSR1), EPH (erythropoietin-producing hepatocellular carcinoma) receptor B4 (EPHB4) is aberrantly overexpressed in human colon tumor cell lines and selectively required for their survival. KSR1 and EPHB4 support tumor cell survival by promoting the expression of downstream targets, Myc and the transcriptional coactivator peroxisome proliferator-activated receptor gamma coactivator 1β (PGC1β). While KSR1 promotes the aberrant expression of Myc and the PGC1β protein via a posttranscriptional mechanism, EPHB4 has a greater effect on Myc and PGC1β expression via its ability to elevate mRNA levels. Subsequent analysis of the posttranscriptional regulation demonstrated that KSR1 promotes the translation of Myc protein. These findings reveal novel KSR1- and EPHB4-dependent signaling pathways supporting the survival of colorectal cancer cells through regulation of Myc and PGC1β, suggesting that inhibition of KSR1 or EPHB4 effectors may lead to selective toxicity in colorectal tumors.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR42411957	EphB4 active human			Price

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