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Updated: Jul 14, 2026

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

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

Published on: August 4, 2019

Activation of p53 by MEG3 non-coding RNA.

Yunli Zhou¹, Ying Zhong, Yingying Wang

¹Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA. yzhou2@partners.org

The Journal of Biological Chemistry

|June 16, 2007

Summary

The maternally expressed gene 3 (MEG3) non-coding RNA acts as a tumor suppressor by activating p53 and inhibiting cell proliferation through both p53-dependent and independent pathways.

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Area of Science:

Molecular Biology
Genetics
Cancer Research

Background:

MEG3 is a maternally expressed imprinted gene.
MEG3 is suggested to function as a non-coding RNA.
MEG3 exhibits tumor suppressor activity.

Purpose of the Study:

To investigate the hypothesis that MEG3 functions through the activation of the tumor suppressor p53.
To elucidate the mechanisms underlying MEG3's tumor suppressor function.

Main Methods:

Transfection of MEG3 expression constructs.
Functional assay using p53-responsive promoter activity.
Analysis of p53 protein levels and transcriptional activity.
Assessment of GDF15 and p21(CIP1) expression.
Investigation of MDM2 levels.
Cell proliferation assays in the presence and absence of p53.

Main Results:

MEG3 transfection significantly increased p53 protein levels and stimulated p53-dependent transcription.
MEG3 functions as a non-coding RNA, with RNA folding being critical for its activity.
MEG3 enhanced p53 binding to the GDF15 promoter, increasing GDF15 expression.
MEG3 selectively regulated p53 transcriptional activity, not inducing p21(CIP1) expression.
MEG3 down-regulated MDM2 levels, contributing to p53 accumulation.
MEG3 inhibited cell proliferation independently of p53.

Conclusions:

MEG3 functions as a tumor suppressor through both p53-dependent and p53-independent mechanisms.
MEG3's non-coding RNA nature is essential for its tumor suppressor activity.
MEG3 influences p53 stability and transcriptional specificity, offering potential therapeutic insights.