# Garcinol as an Epigenetic Modulator: Mechanisms of Anti-Cancer Activity and Therapeutic Potential

## TL;DR

Garcinol, a natural compound, shows promise as an anti-cancer agent by modulating epigenetic processes and inhibiting tumor growth.

## Contribution

This review highlights garcinol's novel role as an epigenetic modulator and HAT inhibitor with potential therapeutic applications.

## Key findings

- Garcinol inhibits histone acetyltransferases (HATs), impacting epigenetic regulation.
- It regulates oncogenic microRNAs and modulates tumor progression pathways in preclinical models.
- Current evidence supports its anti-cancer potential but lacks robust clinical validation.

## Abstract

The limitations of conventional cancer therapies, including toxicity and resistance, underscore the need for safer and more versatile alternatives that can either complement or substitute existing regimens. Garcinol, a polyisoprenylated benzophenone derived primarily from the rind and leaves of Garcinia indica and Garcinia cambogia, has drawn significant interest in recent decades. Although traditionally used to relieve inflammatory disorders, its biomedical relevance expanded considerably after reports in the late 20th century demonstrated antimicrobial and subsequently anti-cancer properties. A growing body of cell-based research, supported by a smaller set of animal experiments, now suggests that garcinol acts as a potent epigenetic modulator. Its activities include inhibition of histone acetyltransferases (HATs), a groundbreaking research followed by regulation of oncogenic microRNAs, and modulation of signaling pathways critical to tumor progression. This review integrates current findings on garcinol’s dual role as a HAT inhibitor and regulator of oncogenic networks with updates on in vitro and in vivo studies with a more focused approach on in vivo animal models, highlighting its potential as an emerging therapeutic against malignancies and inflammatory diseases. Nonetheless, translation into clinical settings remains premature, as robust in vivo evidence is sparse and human trials are lacking. Moving forward, systematic investigations are required to clarify safety profiles, establish effective dosing strategies, and evaluate its efficacy across different cancer types.