# The role and research progress of FGF21 in breast cancer: a review

## TL;DR

This review explores how FGF21 promotes breast cancer growth through metabolic changes and immune evasion, and its potential as a target for treatment.

## Contribution

The paper systematically summarizes FGF21's dual role in metabolism and tumor progression, highlighting new therapeutic strategies.

## Key findings

- FGF21 promotes tumor metastasis by enhancing fatty acid oxidation via the ERK1/2-SENP2-CD36 axis.
- FGF21 induces CD8+ T cell exhaustion through cholesterol synthesis pathways, aiding immune evasion.
- High FGF21 levels correlate with poor prognosis in breast cancer patients, especially those with metabolic disorders.

## Abstract

To investigate the molecular mechanisms, functional controversies, and clinical significance of Fibroblast Growth Factor 21 (FGF21) in the context of breast cancer.

A comprehensive literature search was conducted across databases including PubMed and CNKI to summarize recent advances regarding FGF21 in metabolic reprogramming and immune microenvironment remodeling.

FGF21 primarily serves as a pro-tumorigenic factor in breast cancer through several key mechanisms: (1) Metabolic Reprogramming: It activates the ERK1/2-SENP2 axis to upregulate CD36, which enhances fatty acid oxidation to fuel tumor metastasis. (2) Immune Evasion: It induces CD8+ T cell exhaustion by persistently activating intracellular cholesterol synthesis pathways. (3) Anti-apoptosis: It enhances chemoresistance by activating signaling pathways such as STAT3. Clinically, elevated FGF21 levels are significantly correlated with disease progression and poor prognosis, particularly in patients with metabolic comorbidities.

FGF21 acts as a pivotal bridge connecting systemic metabolism with local tumor behavior. Future research should focus on developing precision intervention strategies that preserve its systemic metabolic benefits while selectively blocking its local oncogenic effects.