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Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

p53 Attenuates the oncogenic Ras-induced epithelial-mesenchymal transition in human mammary epithelial cells

Jianchao Zhang1, Yang Lei, Xiaoge Gao

  • 1The Institute of Genetics and Cytology, Northeast Normal University, Changchun 130024, PR China.

Biochemical and Biophysical Research Communications
|April 16, 2013
PubMed

Insights

Wild type p53 suppresses Ras-induced epithelial-mesenchymal transition (EMT) and stem cell properties by downregulating MEK-ERK signaling. This finding reveals a novel link between p53 and Ras in tumor progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Tumor suppressor p53 inactivation and oncogene Ras activation are critical in cancer development.
  • The role of p53 and Ras in epithelial-mesenchymal transition (EMT), a key process in tumor progression, is not fully understood.

Purpose of the Study:

  • To investigate the intersection between p53 and Ras activity during EMT.
  • To elucidate the function of wild type p53 in suppressing Ras-driven EMT and tumor growth.

Main Methods:

  • In vitro experiments assessing EMT phenotypes and stem cell properties in response to H-Ras(V12) and wild type p53.
  • Analysis of MEK-ERK signaling pathway modulation.
  • In vivo studies using human mammary epithelial cells to evaluate tumor growth inhibition.

Main Results:

  • Increased wild type p53 expression suppressed H-Ras(V12)-induced EMT phenotypes.
  • p53 restrained stem cell properties and downregulated MEK-ERK signaling.
  • p53 inhibited H-Ras(V12)-induced tumor growth in vivo.

Conclusions:

  • This study reveals a novel correlation between the tumor suppressor p53 and the oncogene Ras in regulating the EMT program.
  • p53 acts to inhibit Ras-driven EMT and tumor progression, expanding knowledge on p53's function in cancer.

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