{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T12:12:13Z","timestamp":1789042333592,"version":"build-2803163510"},"reference-count":161,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T00:00:00Z","timestamp":1788998400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Lung cancer remains the leading cause of cancer-related mortality worldwide, with metastasis, therapeutic resistance, and an immunosuppressive TME representing major barriers to successful treatment. Among the chemokine signaling networks implicated in these processes, the CCL2\u2013CCR2 axis has emerged as an important regulator of tumor progression. By orchestrating the recruitment of monocytes, tumor-associated macrophages, myeloid-derived suppressor cells, and other stromal components, this pathway can establish an immune-permissive niche that supports angiogenesis, epithelial\u2013mesenchymal transition, extracellular-matrix remodeling, metastatic dissemination, and resistance to chemotherapy, targeted therapies, and immunotherapy. Mechanistically, CCL2\u2013CCR2 signaling interacts with key oncogenic pathways, including PI3K\/Akt\/mTOR, STAT3, NF-\u03baB, Toll-like receptor signaling, and non-coding RNA-mediated networks, thereby amplifying pro-tumor inflammatory circuits within the lung TME. Although accumulating evidence indicates that the axis can exert context-dependent tumor-suppressive effects under specific biological conditions, such as promoting M1 macrophage recruitment or enhancing antitumor immunity in selected settings, its overall contribution in lung cancer appears predominantly tumor-promoting. This review comprehensively summarizes the molecular mechanisms governing CCL2\u2013CCR2 signaling in primary lung cancer and in lung metastases. We further discuss emerging therapeutic strategies directed at this axis, including CCR2 antagonists, CCL2-neutralizing agents, engineered immune-cell approaches, and rational combinations with immune-checkpoint inhibitors and targeted therapies. Collectively, the current evidence provides a strong biological rationale and preliminary translational support for further investigation of the CCL2\u2013CCR2 axis as a potential therapeutic target and exploratory biomarker in advanced lung cancer. However, clinical validation remains limited, and additional well-designed studies are required to determine whether modulation of this pathway can meaningfully improve patient outcomes.<\/jats:p>","DOI":"10.3389\/fimmu.2026.1871102","type":"journal-article","created":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T11:36:41Z","timestamp":1789040201000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["The CCL2-CCR2 axis in primary lung cancer and pulmonary metastasis: from molecular mechanisms to therapeutic potentials"],"prefix":"10.3389","volume":"17","author":[{"given":"Yujie","family":"Huang","sequence":"first","affiliation":[{"name":"Department of Radiation Oncology, Hubei Cancer Hospital, Tongji Medical College, Huazhong University of Science and Technology","place":["Wuhan, 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