Journal
JOURNAL OF CELLULAR PHYSIOLOGY
Volume 227, Issue 3, Pages 1212-1219Publisher
WILEY-BLACKWELL
DOI: 10.1002/jcp.24025
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Funding
- National Natural Science Foundation [81001126/H1618]
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Genes associated with retinoid-interferon-induced mortality 19 (GRIM-19) was identified as a tumor suppressor protein associated with apoptosis and growth inhibition. Here, we report that the expression levels of GRIM-19 are significantly attenuated in hepatocellular carcinoma (HCC) patients with deteriorating differentiation states, hepatic capsule invasion and microvascular invasion, suggesting the potential role of GRIM-19 not only at the origin but also in the invasive progression of HCCs. To dissect the possible mechanisms by which GRIM-19 regulates tumor cell invasion, we established the hepatic HL-7702 and HCC Huh-7 cell lines stably depleted of GRIM-19. Results show that downregulation of GRIM-19 induces a morphological transformation resembling epithelialmesenchymal transition (EMT) as well as aberrant expression of epithelial and mesenchymal molecular markers. Additionally, these cells lose contact inhibition, a phenomenon of cessation of cell migration in contact with neighboring cells, as assessed by cell imaging, growth curve and S-phase transition in confluent conditions. Conclusion: Our observations demonstrate a novel mechanistic insight into a critical role of GRIM-19 in HCC invasive potential. J. Cell. Physiol. 227: 12121219, 2012. (C) 2011 Wiley Periodicals, Inc.
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