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Mismatch Repair

Mismatch Repair

Genome Copying Errors

Genome Copying Errors

DNA replication is a well-evolved process that copies millions of base pairs with high fidelity during each cell division. Occasionally a wrong base or a long stretch of wrong bases may get added to the daughter strands. If the errors are left unchecked, cells might accumulate several mutations that might endanger their survival. Therefore, the copying errors are checked and repaired at three levels.

Mismatch Repair

Mismatch Repair

Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...

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Stereotactic Atlas-Guided Laser Capture Microdissection of Brain Regions Affected by Traumatic Injury

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Published on: September 11, 2017

Micro-editing mistake translates into a devastating brain tumor.

Dan Dominissini¹, Ninette Amariglio, Gideon Rechavi

¹Cancer Research Center, Chaim Sheba Medical Center, Tel Hashomer, Israel.

The Journal of Clinical Investigation

|October 25, 2012

Summary

This summary is machine-generated.

This study reveals that under-editing of microRNA miR-376a* promotes glioma invasion. Deregulated microRNA editing affects key regulators of glioma migration and invasion, suggesting potential therapeutic targets.

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Area of Science:

Molecular Biology
Oncology
Epigenetics

Background:

RNA modifications, particularly adenosine-to-inosine RNA editing, are frequently altered in cancer.
A direct link between specific RNA editing events and cancer development remains unclear.

Purpose of the Study:

To elucidate the mechanistic role of microRNA (miRNA) editing in glioma progression.
To identify specific miRNA editing events and their downstream targets contributing to glioma invasiveness.

Main Methods:

Analysis of RNA editing patterns in glioma samples.
Investigating the functional impact of altered miR-376a* editing on glioma cell behavior.
Identifying mRNA targets affected by miR-376a* underediting.

Main Results:

Undereiting of miR-376a* was identified as a key factor promoting glioma invasiveness.
This underediting leads to the redirection of miR-376a* targets, influencing cellular processes.
RAP2A and AMFR were identified as critical regulators of glioma migration and invasion affected by miRNA editing.

Conclusions:

Specific microRNA editing defects, like miR-376a* underediting, mechanistically link RNA editing to glioma invasiveness.
Targeting deregulated miRNA editing pathways, including regulators like RAP2A and AMFR, may offer therapeutic strategies for glioma.
Epigenetic mechanisms controlling RNA editing present promising avenues for future cancer therapies.