A Crosstalk Between K ras (Kirsten Rat Sarcoma Viral Oncogene Homologue) and Adherence Molecular Complex Leads to Disassociation of Cells—A Possible Contribution Towards Metastasis in Colorectal Cancer
Shakoori1,4, Bibi Nazia Murtaza,1,2 Shareen Doak,2 Claire Morgan,2 Muhammad Shahid Nadeem,3 Khalid A. Al-Ghanim,4 and Abdul Rauf . 2016
Constitutive activation of mutant K ras (Kirsten rat sarcoma viral oncogene homologue) and disassembly of E-cadherin–catenin complex
(E-cadherin, a-catenin, b-catenin, and g-catenin) play an important role in apoptosis, differentiation, and cell proliferation. In this study, the
expression pattern of K ras and E-cadherin–catenin complex has been evaluated in normal and mutant colorectal cancer cell lines with an
object to determine its impact on disassociation of cells from one another. We addressed the expression analysis of K ras with reference to its
association with adherence molecules in two colorectal cancer cell lines, that is, Caco-2 (wild type K ras served as a control) and DLD1
(heterozygous mutation at codon 13) at message level by qRT-PCR and translational level by western blotting. Compared to the control Caco-2
cell lines, the K ras in DLD1 cell lines showed slightly higher values while a-catenin showed a slight lower (1.3-folds), b-catenin and
E-cadherin showed significantly lower expression (4.2-fold decrease). It can be inferred that a possible cross talk exists between K ras and
adherent junction mediated signalling. Mutation at codon 13 (G to D) leads to the overexpression of K ras and reduced expression of adherent
junction complex resulting in metastasis. J. Cell. Biochem. 9999: 1–6, 2016. © 2016 Wiley Periodicals, Inc.
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