Journal
ONCOTARGET
Volume 7, Issue 22, Pages 32421-32432Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.8718
Keywords
miR-1207-5p; CSF1; macrophage; tumor microenvironment; lung cancer
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Funding
- National Natural Science Foundation of China [81472694, 81171988]
- China 111 Project [111-2-12]
- Ministry of Education [NCET-11-0520]
- Hunan Provincial Natural Science Foundation of China [14JJ2022]
- Fundamental Research Funds for the Central Universities of Central South University [2015zzts100]
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We previously reported that miR-1207-5p can inhibit epithelial-mesenchymal transition (EMT) induced by growth factors such as EGF and TGF-beta, but the exact mechanism is unclear. Here we identified that Colony stimulating factor 1 (CSF1) is a target gene of miR-1207-5p. CSF1 controls the production, differentiation and function of macrophage and promotes the release of proinflammatory chemokines. We showed that miR-1207-5p inhibited lung cancer cell A549 proliferation, migration and invasion in vitro, and suppressed the STAT3 and AKT signalings. miR-1207-5p overexpression can increase HUVEC angiogenesis, and can modulate the M2 phenotype of macrophage. miR-1207-5p also significantly inhibited A549 cells metastasis in a nude mouse xenograft model. miR-1207-5p and CSF1 expression levels and their relationship with lung cancer survival and metastasis status were assayed by means of a lung cancer tissue microarray. Macrophage is an essential part of the tumor microenvironment, thus the miR-1207-5p-CSF1 axis maybe a new regulator of lung cancer development through modulating the tumor microenvironment.
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