| Summary: | It is well-established that tumor-associated macrophages (TAMs) play an important role in breast cancer development. Accumulating evidence suggested that human cathelicidin antimicrobial protein (<i>CAMP</i>), which is mainly expressed in host defense cells such as macrophages, is crucial not only in combating microorganisms but also promoting tumor growth. Here we report the interaction of <i>CAMP</i> with TAMs in breast cancer. <i>CAMP</i> expression was upregulated in cancer tissues and in the circulation of breast cancer patients. Surgical removal of tumor decreased CAMP peptide serum level. Knockdown of <i>CAMP</i> decreased cell proliferation and migration/invasion ability in breast cancer cells. <i>CAMP</i> expression was altered during macrophage M1/M2 polarization and was expressed predominantly in M2 phenotype. In addition, breast cancer cells co-cultured with macrophages upregulated <i>CAMP</i> expression and also increased cancer cell viability. Xenograft tumors reduced significantly upon <i>CAMP</i> receptor antagonist treatment. Our data implicated that <i>CAMP</i> confers an oncogenic role in breast cancer and plays an important role in the tumor microenvironment between TAMs and breast cancer cells, and blocking the interaction between them would provide a novel therapeutic option for this malignant disease.
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