Growth Compensatory Role of Sulindac Sulfide-induced Thrombospondin-1 Linked with ERK1/2 and RhoA GTPase Signaling Pathways

Overview

Journal Life Sci

Publisher Elsevier

Specialties Biochemistry
Biology
Physiology

Date 2008 Feb 12

PMID 18261746

Citations 1

Authors

Yuseok Moon

Jeung Il Kim

Hyun Yang

Thomas E Eling

Affiliations

Soon will be listed here.

Abstract

Previously, we reported that non-steroidal anti-inflammatory drugs (NSAIDs) suppress cellular invasion which was mediated by thrombospondin-1 (TSP-1). As the extending study of the previous observation, we investigated the effect of NSAID-induced TSP-1 on the cellular growth and its related signaling transduction of the TSP-1 production. Among diverse NSAIDs, sulindac sulfide was most potent of inducing the human TSP-1 protein expression. Functionally, induced TSP-1 expression was associated with the growth-compensatory action of NSAID. TSP-1 expression was also elevated by mitogenic signals of ERK1/2 and RhoA GTPase pathway which had also growth-promotive capability after sulindac sulfide treatment. These findings suggest the possible mechanism through which tumor cells can survive the chemopreventive action of NSAIDs or the normal epithelium can reconstitute after NSAID-mediated ulceration in a compensatory way.

Citing Articles

Sulindac sulfide reverses aberrant self-renewal of progenitor cells induced by the AML-associated fusion proteins PML/RARα and PLZF/RARα.

Steinert G, Oancea C, Roos J, Hagemeyer H, Maier T, Ruthardt M PLoS One. 2011; 6(7):e22540.

PMID: 21811629 PMC: 3139642. DOI: 10.1371/journal.pone.0022540.

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