# Plant-Derived Bioactive Compounds in Inflammation-Related Cancers: Mechanisms and Therapeutic Potential

## TL;DR

This review explores how plant-derived compounds can prevent and treat inflammation-related cancers by targeting multiple biological processes.

## Contribution

The paper provides an integrated framework of how plant-derived compounds modulate inflammation-driven cancer mechanisms.

## Key findings

- Plant-derived compounds target inflammation signaling pathways like NF-κB, MAPK, and JAK/STAT.
- These compounds reduce oxidative stress and DNA damage while reprogramming the tumor microenvironment.
- Nanocarrier delivery systems and combination therapies are highlighted for clinical translation.

## Abstract

Chronic inflammation is a well-established driving force in tumor initiation and progression, accounting for a substantial proportion of inflammation-associated malignancies. Persistent inflammatory stimulation creates a pathological microenvironment characterized by sustained inflammatory signaling, oxidative stress, immune dysregulation, and epigenetic reprogramming, which collectively promote genomic instability, malignant transformation, and tumor progression. Understanding the biological basis of inflammation–cancer transformation is therefore essential for the development of effective preventive and therapeutic strategies. Plant-derived bioactive compounds have attracted increasing attention as promising modulators of inflammation-driven carcinogenesis due to their structural diversity, multi-target regulatory capacity, and relatively low toxicity. Specifically, this review focuses on four major classes of these compounds: flavonoids, alkaloids, terpenoids, and curcuminoids. Accumulating evidence demonstrates that these compounds can effectively interrupt the inflammation–cancer continuum by simultaneously targeting multiple pathogenic processes rather than single molecular pathways. In particular, these plant-derived agents suppress inflammation-driven signaling cascades, including NF-κB, MAPK, and JAK/STAT pathways; attenuate oxidative stress and inflammation-induced DNA damage; reprogram the immune microenvironment to restore anti-tumor immunity; and modulate epigenetic and transcriptional programs that stabilize pro-tumorigenic phenotypes. Accordingly, this review synthesizes the shared pathological drivers of inflammation–cancer transformation and summarizes how plant-derived compounds collectively target these mechanisms to interrupt disease progression. In addition, emerging translational strategies, including combination therapy and nanocarrier-based delivery systems, are discussed to highlight the clinical potential of plant-derived interventions. Collectively, this review offers an integrated mechanistic framework for understanding and exploiting plant-derived bioactive compounds in the prevention and treatment of inflammation-related cancers.