• Increases breast tumor proliferation and survival • Reduces cancer cell apoptosis • Elevates tumor cell invasion (including via CCL2 that is released by senescent tumor cells) • Enriches the CSC sub-population • Elevates EMT properties and tumor cell invasion • Promotes endocrine resistance of tumor cells • Reduces the efficacy of immunotherapy • Promotes osteoclast differentiation and bone resorption • Drives forward pro-cancerous tumor-stroma interactions. Here, CCL2 is linked to breast neoplasm.