ArticleJournal of molecular histology2026
CMSS1 promoted CXCL8-CXCR1/2 pathway to accelerate the invasion and immune escape of triple-negative breast cancer.
Article in Journal of molecular histology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
CMSS1, a protein-coding gene, acts as an oncogene in several cancers. However, the role of CMSS1 in triple-negative breast cancer (TNBC) are not clear. Our experiment aims to reveal the biological, prognosis, immunological effects and the underlying mechanism of CMSS1 in TNBC. In this study, CMSS1 expression was markedly up-regulated in tumor tissues of breast cancer than normal tissues. Higher expression of CMSS1 was markedly related with low RFS, shorter overall survival time, later TNM stage and lymph node metastasis. Besides, CMSS1 expression was markedly up-regulated in TNBC cells compared with normal breast epithelial MCF-10 A cells. CMSS1 knockdown repressed the viability and invasion of TNBC cells, inhibited CD8 + T cells apoptosis and decreased PD-L1 expression. Furthermore, CXCL8 overexpression reversed the inhibition effects of CMSS1 on CXCL8, CXCR1, CXCR2 and PD-L1 expression, TNBC cells viability, invasion and apoptosis of CD8 + T cells. Moreover, CMSS1 knockdown repressed tumor volume and weight, decreased PD-L1 expression, promoted CD8 positive staining in xenograft nude mice. Thus, our data verified that CMSS1 was highly expressed in TNBC, and high CMSS1 expression indicated poor prognosis. CMSS1 interference restrained the viability, invasion and immune escape of TNBC cells via CXCL8-CXCR1/2 pathway.
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