ArticleCancer biology & medicine2026
Migration and invasion inhibitory protein inhibits M2 macrophage polarization to suppress colorectal cancer progression through the STING-NFκB2-IL10 axis.
Article in Cancer biology & medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Concurrent sigmoid colon adenocarcinoma presenting with cutaneous adult T-cell leukemia/lymphoma: a rare case report.Infectious agents and cancer · 2026Article
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Abstract
objectiveThis study aimed to determine the role and mechanism underlying migration and invasion inhibitory protein (MIIP) modulation in M2 macrophages within the tumor microenvironment and the potential of targeting the MIIP- stimulator of interferon genes (STING) pathway in colorectal cancer (CRC) therapy.
methodsMIIP expression was analyzed for associations with the STING pathway and M2 macrophage infiltration using public datasets and clinical CRC samples. CRC cells were genetically modified using lentiviral vectors to overexpress or silence MIIP and STING. The interactions of genetically modified CRC cells with macrophages were studied in co-culture systems. Techniques, including immunofluorescence staining, RT-qPCR, western blot, ELISA, flow cytometry, and Transwell migration and invasion assays, were used to evaluate the crosstalk between CRC cells and macrophages. An orthotopic mouse CRC model was developed to study the effects of MIIP on M2 macrophage polarization and tumor metastasis through the STING-NFκB2-IL10 axis. The therapeutic significance of a STING antagonist was also assessed
resultsAnalyses of The Cancer Genome Atlas (TCGA) cohort and our CRC cohort revealed low MIIP expression is associated with STING pathway activation, increased M2 macrophage infiltration, and poor clinical outcomes. The results of functional experiments demonstrated that MIIP inhibits IL10 production
conclusionsThis study established MIIP as a crucial regulator of macrophage polarization in the CRC tumor microenvironment, providing new insights into the role in suppressing CRC progression and immune-tumor crosstalk. These findings highlight the potential of targeting the STING pathway as a therapeutic strategy for CRC patients who respond poorly to immune checkpoint inhibitors.
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