Fig. 5: Co-culture with hADSC cells increased the expression of MMP7/MMP9 in TNBC cells and inhibited the STAT3/NF-κB pathway to weaken the invasion and migration ability of TNBC cells.

MDA-MB-468 and MDA-MB-231 cells were cultured alone or co-cultured with hADSC cells. Add inhibitors for JAK (WWP1066, 2.3 μM) or PBS to the culture medium. A, B 3 days later, TNBC cells were collected to detect the migration and invasion abilities; C–G 3 days later, TNBC cells were collected to detect the expression of proteins related to STAT3 / NF-κB p65 pathway by Western blotting and immunofluorescence; H–J 3 days later, TNBC cells were collected to detect the expression of proteins of MMP7/MMP9 by Western blotting and immunofluorescence. K IL-6-mediated adipocyte microenvironment can activate STAT3/NF-κB pathway and regulate the expression of CXCL1. L Adipocyte-derived IL-6 and TNBC cell-derived CXCL1 co-mediate the interaction mechanism. Adipocyte-derived IL6 activates STAT3/NF-κB pathway in TNBC cells to promote the expression and secretion of CXCL1 in TNBC and promote tumor progression. Tumor-derived CXCL1 further activates STAT3/NF-κB pathway in adipocytes to promote IL6 expression and secretion in adipocytes, and finally forms a cascade of interaction.