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Related Experiment Video

Updated: Jan 17, 2026

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

RAD51-mediated homologous recombination is a pro-tumour driver pathway.

Bernard S Lopez¹

¹Université de Paris-Cité, INSERM U1016, UMR 8104 CNRS, Institut Cochin, Paris, France. bernard.lopez@inserm.fr.

|September 24, 2025

Summary

Homologous recombination (HR) is thought to suppress tumors, but this study suggests HR/RAD51 actually promotes cancer progression by aiding cancer cells in overcoming replication stress. This challenges the established view of HR as a tumor suppressor pathway.

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Real-time Observation of the DNA Strand Exchange Reaction Mediated by Rad51

Real-time Observation of the DNA Strand Exchange Reaction Mediated by Rad51

Published on: February 13, 2019

Area of Science:

Genetics
Cancer Biology
Molecular Oncology

Background:

Homologous recombination (HR) is crucial for genome stability and DNA repair, and is considered a tumor suppressor pathway.
Mutations in HR genes are common in cancers, yet RAD51, central to HR, lacks associated cancer predisposition mutations (the "RAD51 paradox").
This paradox suggests cancer predisposition might stem from alternative mutagenic repair pathways activated by HR deficiency, rather than HR deficiency itself.

Purpose of the Study:

To investigate whether HR deficiency or alternative repair pathways drive cancer predisposition.
To re-evaluate the role of RAD51-controlled HR in tumorigenesis and cancer progression.

Main Methods:

A mouse model was utilized to assess the impact of decreased RAD51 HR activity.
The study specifically modulated HR activity without stimulating alternative repair pathways like single-strand annealing (SSA) or alternative end-joining (A-EJ).

Main Results:

Decreasing RAD51 HR activity in vivo, without promoting SSA or A-EJ, did not favor tumorigenesis and instead appeared protective against it.
These findings contradict the notion that HR acts as a tumor suppressor pathway.

Conclusions:

RAD51-controlled HR facilitates cancer progression, particularly in highly proliferative cancer cells coping with replication stress.
The study proposes that HR/RAD51 aids cancer progression from early hyperplastic states, challenging the long-held dogma of HR as a tumor suppressor.