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Related Experiment Video

Updated: Nov 22, 2025

Live-imaging of Breast Epithelial Cell Migration After the Transient Depletion of TIP60

Live-imaging of Breast Epithelial Cell Migration After the Transient Depletion of TIP60

Published on: December 7, 2017

PRMT5 and Tip60 Modify FOXP3 Function in Tumor Immunity.

Peeyush N Goel¹, Payal Grover¹, Mark I Greene¹

¹Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104.

Critical Reviews in Immunology

|January 11, 2021

Summary

This summary is machine-generated.

Protein arginine methylation by PRMT5 regulates tumor immunity and T regulatory cell function. Targeting PRMT5 offers a promising strategy for effective human cancer treatment by enhancing anti-tumor responses.

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Area of Science:

Molecular Biology
Immunology
Oncology

Background:

Posttranslational modifications (PTMs), including protein arginine methylation, regulate critical cellular processes like DNA damage response and immune signaling.
Protein arginine methyltransferases (PRMTs) are implicated in various diseases due to their dysregulation.
PRMT5, a key arginine methyltransferase, plays a significant role in cancer progression.

Purpose of the Study:

To review the regulation, biological functions, and therapeutic strategies targeting PRMT5.
To focus on the role of PRMT5 in modulating tumor immunity.

Main Methods:

Review of existing literature on PRMT5.
Analysis of PRMT5's regulatory mechanisms, including protein interactions, PTMs, and noncoding RNAs.
Examination of PRMT5's impact on immune cells and cancer progression.

Main Results:

PRMT5 inhibition or deletion enhances tumor immunity by affecting Tip60 histone acetyltransferase activity and FOXP3 levels.
PRMT5 limits the suppressive functions of T regulatory (Treg) cells.
PRMT5 regulates Tip60 expression, which is crucial for FOXP3's DNA interactions.

Conclusions:

PRMT5 is a critical regulator of tumor immunity and Treg cell function.
Targeting PRMT5 presents a viable therapeutic approach for treating human cancers.
Ongoing development of PRMT5 inhibitors shows promise for clinical application.