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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.v2.i1.90
pages 79-87

RKIP-1 and the Cell Cycle: Novel Insight Into Genomic Instability

Fahd Al-Mulla
Faculty of Medicine, Department of Pathology, Kuwait University Health Sciences Centre, Safat, Kuwait

SINOPSIS

RKIP-1 has emerged as a significant metastasis suppressor in various cancers. Loss or reduced RKIP-1 expression has been well documented in aggressive and malignant cancers. In addition, recent data have stipulated a potential prognostication utility for the RKIP-1 expression level in colorectal, prostate, and gastrointestinal stromal tumors. This repressor and scaffold protein appear to be involved in a wide variety of intracellular signaling cascades ranging from the inhibition of Raf-1/MEK/ERK to the activation of the G protein–coupled receptor signaling pathway. However, its role in cellular growth, the cell cycle, and genomic instability has received little attention, especially in primary and immortalized (noncancerous) cells. We demonstrated that RKIP-1 depletion in HEK-293 cells caused a dramatic fast-forwarding or acceleration in the cell cycle at the S- and G2M phases, which may be a consequence to alteration in key cell cycle checkpoint proteins, such as Aurora B and NEK 6. Our data also demonstrate an increased trend for homozygosity accumulation after long-term culture of RKIP-1–depleted HEK-293 cells. This novel finding might have important ramifications to cancer development, particularly in the inactivation of tumor suppressor genes.


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