ArticleBreast cancer research : BCR2025
Chemoresistant tumor cell secretome potentiates immune suppression in triple negative breast cancer.
Article in Breast cancer research : BCR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Hesperetin-black phosphorus nanosheets targeting TAMs induce ferroptosis and reverse protumoral polarization to remodel the immune microenvironment.Materials today. Bio · 2026Article
- Breast Cancer Milieu Maneuvers Cancer-Associated Macrophages to Synergize Neoplastic Repertoires.Cancers · 2026Review
- Contribution of Mesenchymal-like and Epithelial Cellular Subsets to Chemotherapy Resistance in Triple-Negative Breast Cancer.International journal of molecular sciences · 2026Article
- Single-Cell Analysis Links C7+ Cancer-Associated Fibroblasts with Incomplete Resection in Platinum-Sensitive Relapsed Ovarian Cancer.Biomedicines · 2025Article
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Abstract
backgroundChemotherapy is an integral part of the clinical management of triple negative breast cancer (TNBC), however, development of chemoresistance occurs frequently. Tumor sensitivity to treatment is known to be strongly influenced by the immune microenvironment, signifying the predictive potential of immune alterations. How tumor cells that acquire resistance may subsequently modulate the immune microenvironment it is still not well described. Here, we investigated immunomodulation in the context of acquired chemoresistance in TNBC, focusing on the role of the secretome.
methodsBulk RNA sequencing and multiplex cytokine profiling were performed on paclitaxel-resistant and -sensitive isogenic variants of TNBC cells to reveal resistance-associated secretome alterations. The immunomodulatory influence of the tumor cell secretome was investigated by exploring its effect on monocytes, macrophages (MΦs) and T cells derived from healthy blood donors. The influence on the immune cell phenotype and activity was evaluated by measuring molecular markers and performing functional assays. To validate the clinical relevance, we utilized longitudinal -omics data from breast cancer patients refractory to standard chemotherapy in the NeoAva clinical trial. CIBERSORT was applied to transcriptomics data to infer MΦ and T cell abundance in individual tumors upon treatment. To evaluate their association with the secretome profiles, patient-matched serum cytokine data were used.
resultsThe acquisition of chemoresistance was accompanied by enhanced secretion of cytokines. Subsequently, the resistant cell secretome affected the abundance, phenotype and activity of immune cells. Specifically, it potentiated the recruitment of monocytes, facilitated the polarization of MΦs towards the immunosuppressive M2-like phenotype, and attenuated the activation of CD8
conclusionDevelopment of chemoresistance in BC is associated with alterations in the tumor secretome, which impairs immune activation and facilitates immunosuppression. Knowledge on the immune microenvironment in residual tumors after standard chemotherapy could aid in selecting rational treatment options for this group of patients.
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