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Updated: Jun 12, 2025

Yeast As a Chassis for Developing Functional Assays to Study Human P53
Published on: August 4, 2019
Decoding the molecular symphony: interactions between the m6A and p53 signaling pathways in cancer
Rachel Shoemaker1,2, Mo-Fan Huang1,2, Ying-Si Wu1,3
1Department of Integrative Biology and Pharmacology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Abstract:
The p53 tumor suppressor gene governs a multitude of complex cellular processes that are essential for anti-cancer function and whose dysregulation leads to aberrant gene transcription, activation of oncogenic signaling and cancer development. Although mutations can occur at any point in the genetic sequence, missense mutations comprise the majority of observed p53 mutations in cancers regardless of whether the mutation is germline or somatic. One biological process involved in both mutant and wild-type p53 signaling is the N 6-methyladenosine (m6A) epitranscriptomic network, a type of post-transcriptional modification involved in over half of all eukaryotic mRNAs. Recently, a significant number of findings have demonstrated unique interactions between p53 and the m6A epitranscriptomic network in a variety of cancer types, shedding light on a previously uncharacterized connection that causes significant dysregulation. Cross-talk between wild-type or mutant p53 and the m6A readers, writers and erasers has been shown to impact cellular function and induce cancer formation by influencing various cancer hallmarks. Here, this review aims to summarize the complex interplay between the m6A epitranscriptome and p53 signaling pathway, highlighting its effects on tumorigenesis and other hallmarks of cancer, as well as identifying its therapeutic implications for the future.
Insights
The p53 tumor suppressor and the N6-methyladenosine (m6A) epitranscriptomic network interact, influencing cancer development. Understanding this cross-talk offers new therapeutic strategies for cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- The p53 tumor suppressor gene is crucial for anti-cancer functions.
- Dysregulation of p53 signaling, often through missense mutations, contributes to cancer development.
- The N6-methyladenosine (m6A) epitranscriptomic network, a key post-transcriptional modification, influences numerous cellular processes.
Purpose of the Study:
- To review the intricate relationship between the p53 signaling pathway and the m6A epitranscriptome.
- To elucidate how this interplay affects tumorigenesis and cancer hallmarks.
- To identify potential therapeutic implications arising from this interaction.
Main Methods:
- Literature review synthesizing recent findings on p53 and m6A interactions.
- Analysis of studies investigating the impact of wild-type and mutant p53 on m6A regulators (readers, writers, erasers).
- Examination of how these interactions influence cancer hallmarks and cellular functions.
Main Results:
- Significant interactions between p53 (both wild-type and mutant forms) and the m6A network have been identified across various cancer types.
- Cross-talk between p53 and m6A regulators impacts gene transcription, oncogenic signaling, and cellular processes.
- This interaction influences key cancer hallmarks, contributing to tumor formation and progression.
Conclusions:
- The interplay between p53 and the m6A epitranscriptome represents a critical, previously underappreciated, mechanism in cancer.
- Targeting this interaction holds promise for novel cancer therapeutic strategies.
- Further research into this molecular axis is warranted for clinical translation.
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