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CCR2 Chemokine Receptors Enhance Growth and Cell-Cycle Progression of Breast Cancer Cells through SRC and PKC Activation. | LitMetric

AI Article Synopsis

  • Basal-like breast cancers are a highly aggressive subtype of breast cancer that often lack key hormone receptors and have limited treatment options, making research into their progression essential for developing new therapies.
  • The CCL2/CCR2 chemokine pathway is crucial for regulating inflammation and tumor growth in basal-like breast cancers, with significant roles demonstrated in both breast cancer cells and their surrounding fibroblasts.
  • Inhibition of CCL2/CCR2 signaling through gene modification reduces tumor growth and alters cell proliferation by affecting vital proteins like p27KIP1, indicating that this pathway could serve as a potential therapeutic target.

Article Abstract

Basal-like breast cancers are an aggressive breast cancer subtype, which often lack estrogen receptor, progesterone receptor, and Her2 expression, and are resistant to antihormonal and targeted therapy, resulting in few treatment options. Understanding the underlying mechanisms that regulate progression of basal-like breast cancers would lead to new therapeutic targets and improved treatment strategies. Breast cancer progression is characterized by inflammatory responses, regulated in part by chemokines. The CCL2/CCR2 chemokine pathway is best known for regulating breast cancer progression through macrophage-dependent mechanisms. Here, we demonstrated important biological roles for CCL2/CCR2 signaling in breast cancer cells. Using the MCF10CA1d xenograft model of basal-like breast cancer, primary tumor growth was significantly increased with cotransplantation of patient-derived fibroblasts expressing high levels of CCL2, and was inhibited with CRISP/R gene ablation of stromal . CRISP/R gene ablation of in MCF10CA1d breast cancer cells inhibited breast tumor growth and M2 macrophage recruitment and validated through CCR2 shRNA knockdown in the 4T1 model. Reverse phase protein array analysis revealed that cell-cycle protein expression was associated with CCR2 expression in basal-like breast cancer cells. CCL2 treatment of basal-like breast cancer cell lines increased proliferation and cell-cycle progression associated with SRC and PKC activation. Through pharmacologic approaches, we demonstrated that SRC and PKC negatively regulated expression of the cell-cycle inhibitor protein p27KIP1, and are necessary for CCL2-induced breast cancer cell proliferation. IMPLICATIONS: This report sheds novel light on CCL2/CCR2 chemokine signaling as a mitogenic pathway and cell-cycle regulator in breast cancer cells.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6359961PMC
http://dx.doi.org/10.1158/1541-7786.MCR-18-0750DOI Listing

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