# Insight into the mechanisms and dysregulation of KMT5C-H4K20me3 in cancer

## TL;DR

This review explores how KMT5C and H4K20me3 are involved in cancer, highlighting new pathways and potential for targeted therapies.

## Contribution

The paper introduces a novel, non-canonical pathway for H4K20me3 deposition by KMT5C and suggests future therapeutic opportunities.

## Key findings

- KMT5C-H4K20me3 is linked to cancer and genome integrity.
- A non-canonical pathway for H4K20me3 deposition by KMT5C is suggested.
- Dysregulation of KMT5C-H4K20me3 presents therapeutic potential.

## Abstract

KMT5C-mediated histone H4 lysine 20 trimethylation (H4K20me3) has traditionally been linked to heterochromatin formation and maintenance, playing a crucial role in maintaining genome integrity. Emerging evidence, however, indicates that perturbations of KMT5C-H4K20me3 are also implicated in various cancers, positioning KMT5C-H4K20me3 as a promising target for anti-cancer therapies. Despite this, the precise mechanisms underlying KMT5C recruitment to its genomic targets and the specific genes it regulates remain poorly understood. In this review, we explore the dysregulation of KMT5C-mediated H4K20me3 in cancer, providing a comprehensive overview of its known functions. We also highlight recent findings that suggest a novel, non-canonical pathway for H4K20me3 deposition by KMT5C, and, while early on, insight into future opportunities for therapeutic intervention.