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Forum on Immunopathological Diseases and Therapeutics
SJR: 0.309 SNIP: 0.041 CiteScore™: 0.18

ISSN Imprimir: 2151-8017
ISSN En Línea: 2151-8025

Archives: Volume 1, 2010 to Volume 7, 2016

Forum on Immunopathological Diseases and Therapeutics

DOI: 10.1615/ForumImmunDisTher.2016017232
pages 107-118

Regulation of the Cancer Stem Cell Phenotype by Raf Kinase Inhibitor Protein via Its Association with Kruppel-Like Factor 4

Stephanie Wottrich
Department of Microbiology, Immunology, and Molecular Genetics, David Geffen School of Medicine, Jonsson Comprehensive Cancer Center, University of California, Los Angeles, CA 90095
Benjamin Bonavida
Department of Microbiology, Immunology, & Molecular Genetics, David Geffen School of Medicine, Johnson Comprehensive Cancer Center, University of California at Los Angeles, Los Angeles, CA 90025-1747

SINOPSIS

As one of four core transcription factors whose expression is required to induce the pluripotent state, Kruppel-like factor 4 (KLF4) is a factor of utmost interest to the medical scientific community. Particularly, since the discovery of its unusual capability as an indispensable player along with three other factors in achieving this state, significant research has been conducted regarding unearthing the mechanisms by which KLF4 is required for cells to achieve such a state of plasticity. As dynamic as it is, however, the mechanism by which KLF4 carries out its functions is rooted in a number of different systematic regulatory pathways, such as immune function and wound healing among others, including its recently discovered roles that give rise to the embryonic stem cell phenotype and the cancer stem cell (CSC) phenotype. There is a sensitive equilibrium between KLF4 and other proteins as well as epigenetic factors and signals that determine the overall outcome of the functions of KLF4. However, as of yet, very few defined mechanistic pathways fully explain how and why KLF4 contributes specifically to the CSC phenotype. Instead, what is known is based largely on general trends and conjectural implications. The contrasting properties between KLF4 and the metastasis suppression and reversal of drug resistance mediated by Raf kinase inhibitor protein (RKIP) have led us to hypothesize that there might be cross talk between KLF4 and RKIP in CSCs. This brief review presents an overview of some studies reporting on the important role of RKIP in the regulation of the CSC phenotype via its association with KLF4.

PALABRAS CLAVE: cell signaling, CSCs, EMT, KLF4, RKIP

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