# DUSP1: Triple-Negative Breast Cancer and Therapeutic Potential

## TL;DR

This paper reviews how DUSP1 influences triple-negative breast cancer progression and treatment resistance, highlighting its potential as a therapeutic target.

## Contribution

The paper provides a synthesis of DUSP1's context-dependent role in TNBC, focusing on chemotherapy resistance and immunotherapy implications.

## Key findings

- Reduced DUSP1 expression correlates with aggressive TNBC phenotypes and poor prognosis.
- Therapy-induced DUSP1 upregulation can promote resistance to chemotherapy and radiotherapy.
- DUSP1 modulates the tumor microenvironment and affects immunotherapy response in TNBC.

## Abstract

Triple negative breast cancer (TNBC) is an aggressive and highly metastatic cancer that shows therapy resistance and poor prognosis in breast cancer patients. Due to the lack of expression of estrogen, progesterone, and HER2 receptors, hormonal therapy is unable to target TNBC and mostly relies on chemotherapy, radiotherapy, and immunotherapy as treatment options in the clinic. Downregulation of dual-specificity protein phosphatase 1 (DUSP1/MKP-1) in TNBC may promote TNBC cell proliferation and metastasis by activation of mitogen-activated protein kinases (MAPKs). In this brief review, we analyzed the expression profile of DUSP1 and discussed its correlation, significance, and therapeutic potential in TNBC with the current literature.

Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype characterized by high rates of recurrence, limited targeted treatment options, and frequent resistance to standard therapies. Dual-specificity protein phosphatase 1 (DUSP1), a stress-responsive regulator of mitogen-activated protein kinase (MAPK) signaling, has emerged as a context-dependent modulator of tumor progression and therapeutic response in TNBC. While reduced DUSP1 expression has been associated with aggressive tumor phenotypes and poor prognosis, accumulating evidence indicates that therapy-induced upregulation of DUSP1 can promote resistance to chemotherapy and radiotherapy by attenuating pro-apoptotic MAPK signaling and fostering immunosuppressive tumor microenvironment (TME). Emerging evidence highlights that DUSP1’s role is context-dependent on human cancers, including breast cancer (BC). This review synthesizes current evidence on DUSP1 biology in TNBC, with emphasis on its mechanistic involvement in chemotherapy resistance, radiation-induced immune modulation, and emerging implications for immunotherapy response.