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Lowered Expression of Tumor Suppressor Candidate MYO1C Stimulates Cell Proliferation, Suppresses Cell Adhesion and Activates AKT

Journal article
Authors Kittichate Visuttijai
Jennifer Pettersson
Y. M. Azar
I. van den Bout
C. Orndal
Janusz Marcickiewicz
Staffan Nilsson
M. Hornquist
B. Olsson
K. Ejeskar
A. Behboudi
Published in Plos One
Volume 11
Issue 10
Pages e0164063
ISSN 1932-6203
Publication year 2016
Published at Institute of Biomedicine, Department of Medical and Clinical Genetics
Department of Mathematical Sciences, Applied Mathematics and Statistics
Pages e0164063
Language en
Links dx.doi.org/10.1371/journal.pone.016...
Subject categories Biological Sciences

Abstract

Myosin-1C (MYO1C) is a tumor suppressor candidate located in a region of recurrent losses distal to TP53. Myo1c can tightly and specifically bind to PIP2, the substrate of Phosphoinositide 3-kinase (PI3K), and to Rictor, suggesting a role for MYO1C in the PI3K pathway. This study was designed to examine MYO1C expression status in a panel of well-stratified endometrial carcinomas as well as to assess the biological significance of MYO1C as a tumor suppressor in vitro. We found a significant correlation between the tumor stage and lowered expression of MYO1C in endometrial carcinoma samples. In cell transfection experiments, we found a negative correlation between MYO1C expression and cell proliferation, and MYO1C silencing resulted in diminished cell migration and adhesion. Cells expressing excess of MYO1C had low basal level of phosphorylated protein kinase B (PKB, a. k. a. AKT) and cells with knocked down MYO1C expression showed a quicker phosphorylated AKT (pAKT) response in reaction to serum stimulation. Taken together the present study gives further evidence for tumor suppressor activity of MYO1C and suggests MYO1C mediates its tumor suppressor function through inhibition of PI3K pathway and its involvement in loss of contact inhibition.

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