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Tumor-associated Macrophages Activated by Leptin Promote Migration and Invasion of Breast Cancer MCF7 Cells
Cao Hong, Wang Lin, Pang Xueli, Li Kuangfa, Su Min, Huang Yunxiu, Wei Lan, Chen Tingmei*
Key Laboratory of Laboratory Medical Diagnostics, Ministry of Education; College of Laboratory Medicine,Chongqing Medical University, Chongqing 400016, China
Abstract: This paper investigated the effect of tumor-associated macrophages activated by leptin on migration and invasion of MCF7 cells and explored its molecule mechanisms. The expressions of CD206， TGF-β and IL-10 were detected by RT-PCR， FQ-PCR and Western blot. Ob-Rb and Ob-Rt in TAMs were detected by RT-PCR. The migration and invasion of MCF7 cells were determined by cell scratch assay and Transwell chamber assay. The expressions of p-STAT3， p-ERK 1/2 and p-AKT in TAMs were detected by Western blot. The mRNA and protein expression of MMP2 and MMP9 in TAMs were detected by RT-PCR and Western blot. The results suggested that the phenotype of macrophage induced by PMA (100 nmol/L) and IL-4 (20 ng/mL) was CD206+TGF-βHighIL-10High. The conditional medium of TAMs activated by leptin significantly increased the migration and invasion of MCF7 cells. The expressions of p-STAT3， p-ERK 1/2 and p-AKT in TAMs were significantly enhanced by leptin (P<0.05). Furthermore， the mRNA and protein expressions of MMP2 and MMP9 in TAMs were remarkably up-regulated by leptin (P<0.05). However， the MAPK/ERK 1/2 inhibitor PD98059 could down-regulate the expression of MMP2 in TAMs treated with leptin (P<0.05)， and JAK/STAT inhibitor AG490 could decrease the expression of MMP9 (P<0.05). In conclusion， leptin can enhance the migration and invasion of MCF7 cells via activating TAMs， which may be associated with the up-regulation of MMP2 and MMP9 in TAMs， through MAPK/ERK 1/2 and JAK/STAT signaling pathways， respectively.
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