# Molecular mechanisms governing the differentiation and expansion of myeloid-derived suppressor cells

**Authors:** Ke Wang, Xiao Wang, Nan Sun

PMC · DOI: 10.3389/fcell.2025.1677201 · 2025-10-17

## TL;DR

This paper reviews how myeloid-derived suppressor cells develop and expand, focusing on their role in cancer immune evasion and potential therapeutic targets.

## Contribution

The paper provides a comprehensive review of signaling pathways and regulatory factors governing MDSC differentiation and expansion.

## Key findings

- Key signaling pathways like JAK/STAT, NF-κB, and Notch are central to MDSC biology.
- Regulatory cytokines, metabolic factors, and epigenetic modifications influence MDSC development.
- Understanding these mechanisms can lead to novel cancer immunotherapies targeting MDSC-mediated immunosuppression.

## Abstract

Myeloid-derived suppressor cells (MDSCs) play critical roles in tumor immune evasion. These heterogeneous cells are broadly classified into granulocytic (G-MDSC), monocytic (M-MDSC), and their immature precursors, early-stage MDSCs (e-MDSCs). Elucidating their differentiation and expansion mechanisms is crucial for advancing cancer immunotherapy. This review examines the key signaling pathways (e.g., JAK/STAT, NF-κB, Notch), regulatory cytokines, metabolic factors, and epigenetic modifications central to MDSC biology. A comprehensive understanding of these intricate networks provides valuable insights into tumor immune evasion and facilitates the identification of novel therapeutic targets designed to overcome MDSC-mediated immunosuppression.

## Linked entities

- **Proteins:** NFKB1 (nuclear factor kappa B subunit 1), Notch (neurogenic locus notch homolog)
- **Diseases:** cancer (MONDO:0004992)

## Full-text entities

- **Genes:** NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}
- **Diseases:** cancer (MESH:D009369)

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12575322/full.md

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Source: https://tomesphere.com/paper/PMC12575322