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MCT-1/miR-34a/IL-6/IL-6R signaling axis promotes EMT progression, cancer stemness and M2 macrophage polarization in triple-negative breast cancer
Open accessAbstract
BACKGROUND: Triple-negative breast cancer (TNBC) is a poor prognostic breast cancer with the highest mutations and limited therapeutic choices. Cytokine networking between cancer cells and the tumor microenvironment (TME) maintains the self-renewing subpopulation of breast cancer stem cells (BCSCs) that mediate tumor heterogeneity, resistance and recurrence. Immunotherapy of those factors combined with targeted therapy or chemoagents may advantage TNBC treatment. RESULTS: We found that the oncogene Multiple Copies in T-cell Malignancy 1 (MCT-1/MCTS1) expression is a new poor-prognosis marker in patients with aggressive breast cancers. Overexpressing MCT-1 perturbed the oncogenic breast epithelial acini morphogenesis and stimulated epithelial-mesenchymal transition and matrix metalloproteinase activation in invasive TNBC cells, which were repressed after MCT-1 gene silencing. As mammary tumor progression was promoted by oncogenic MCT-1 activation, tumor-promoting M2 macrophages were enriched in TME, whereas M2 macrophages were decreased and tumor-suppressive M1 macrophages were increased as the tumor was repressed via MCT-1 knockdown. MCT-1 stimulated interleukin-6 (IL-6) secretion that promoted monocytic THP-1 polarization into M2-like macrophages to increase TNBC cell invasiveness. In addition, MCT-1 elevated the soluble IL-6 receptor levels, and thus, IL-6R antibodies antagonized the effect of MCT-1 on promoting M2-like polarization and cancer cell invasion. Notably, MCT-1 increased the features of BCSCs, which were further advanced by IL-6 but prevented by tocilizumab, a humanized IL-6R antibody, thus MCT-1 knockdown and tocilizumab synergistically inhibited TNBC stemness. Tumor suppressor miR-34a was induced upon MCT-1 knockdown that inhibited IL-6R expression and activated M1 polarization. CONCLUSIONS: The MCT-1 pathway is a novel and promising therapeutic target for TNBC.
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Cited by
Cancer stem cell (CSC) resistance drivers
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Emerging role of tumor cell plasticity in modifying therapeutic response
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Metadata
- Authors
- Weng, Y.-S., Tseng, H.-Y., Chen, Y.-A., Shen, P.-C., Al Haq, A. T., Chen, L.-M., Tung, Y.-C., & Hsu, H.-L.
- Venue
- Molecular Cancer
- Published
- 2019-03-18
- Volume
- 18
- Issue
- 1
- Pages
- 42-42
- ISSN
- 1476-4598 (ISSN-L)
- OpenAlex
- W2939212581
- Cited by
- 444
- References
- 50
- FWCI
- 17.32
- Type
- journal article
- Language
- en
- Open access
- gold
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- Weng, Y.-S., Tseng, H.-Y., Chen, Y.-A., Shen, P.-C., Al Haq, A. T., Chen, L.-M., Tung, Y.-C., & Hsu, H.-L. (2019). MCT-1/miR-34a/IL-6/IL-6R signaling axis promotes EMT progression, cancer stemness and M2 macrophage polarization in triple-negative breast cancer. Molecular Cancer. https://doi.org/10.1186/s12943-019-0988-0
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