a-simplified-robust-protocol-for-isolation-long-term-expansion

A Simplified and Robust Protocol for the Isolation and Long-term Expansion of Primary Human Endometrial Epithelial Cells

Research on endometrial disorders, including tamoxifen-associated endometrial hyperplasia, has been limited by the lack of robust in vitro epithelial ...

The First Clinical Medical College of Zhejiang Chinese Medical University

Mitogen-activated protein kinase phosphatases (MKPs), also known as dual-specificity phosphatases (DUSPs), are key regulatory factors within the mitogen-activated protein kinase (MAPK) pathway. MKP7/DUSP16, a member of the MKP family, has been identified in vitro as a phosphatase with specificity for p38 mitogen-activated protein kinase (p38) and c-jun amino-terminal kinase (JNK), with a stronger inhibitory effect on JNK compared to other MAPKs. In recent years, MKP7/DUSP16 has recently attracted increasing interest, with accumulating evidence suggesting its dysfunction is correlated with the progression and drug resistance of various cancers, making it a potential prognostic biomarker. However, research into the specific mechanisms by which MKP7/DUSP16 regulates cancer cells remains limited. Current studies suggest that MKP7/DUSP16 may promote cancer progression through the regulation of the MAPK pathway, mitochondrial apoptosis pathways, and the induction of cancer cell proliferation by immune cells. This review summarizes the mechanisms by which MKP7/DUSP16 may promote tumor proliferation. Further studies are needed to clarify its specific regulatory roles in cancer.

Regulatory roles of MKP7/DUSP16 in cancer.

Breast cancer remains the most commonly diagnosed cancer among women worldwide, and multiple studies now link its development and progression to disturbances in metabolic and immune regulation. Among these factors, the gut microbiota is increasingly recognized as a modulator of host physiology through its metabolism of dietary tryptophan (Trp). Here we focus on the current understanding of the microbial metabolism of Trp, which primarily generates bioactive metabolites through the kynurenine (Kyn) pathway and the indole pathway. These metabolites can serve as endogenous ligands, activating the aryl hydrocarbon receptor (AhR) signaling pathway. They can also promote tumor stem cell characteristics, epithelial-mesenchymal transition (EMT), and metastasis  serotonin receptors (such as HTR1B/1D, HTR2B). The activation of such pathways contributes to the remodeling of the tumor immune microenvironment, alters the functions of immune cells, and directly influences the proliferation, invasion, and metastatic behavior of breast cancer cells. By integrating findings from preclinical and clinical studies, this review organizes current evidence around the "gut microbiota-Trp metabolism-breast cancer" axis and discusses clinical implications and current limitations. Targeting this metabolic network may provide new opportunities for breast cancer prevention and therapeutic intervention.

Article	Year
Regulatory roles of MKP7/DUSP16 in cancer. Medical oncology (Northwood, London, England)\| PubMed ID: 41320681	2025
Gut microbiota-regulated tryptophan metabolism in breast cancer: mechanisms and therapeutic perspectives. Frontiers in oncology\| PubMed ID: 41821883	2026

Xuanwei Wu

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