Article ID Journal Published Year Pages File Type
10759154 Biochemical and Biophysical Research Communications 2013 8 Pages PDF
Abstract
Inactivation of the tumor suppressor p53 and activation of the oncogene Ras are the two most pivotal events in tumor development. However, potential intersection between p53 and Ras activity during an EMT process, which plays a crucial role during malignant tumor progression, remains elusive. Here, we report that increased expression of wild type p53 suppressed H-RasV12-induced EMT phenotypes and restrained stem cell properties, through downregulation of MEK-ERK signaling pathways. In vivo experiments showed that p53 was able to inhibit H-RasV12-induced tumor growth of human mammary epithelial cells. This study elucidates a novel correlation between the tumor suppressor gene p53 and the oncogene Ras in regulating EMT program, and expands the knowledge about the function of p53 in EMT process.
Related Topics
Life Sciences Biochemistry, Genetics and Molecular Biology Biochemistry
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