Fig. 5

PI3K/AKT signaling pathway, rather than JAK/STAT3 signaling pathway that contributes to PLOD2 activation in CAAs. a,b Adipocytes were cultivated in the presence or in the absence of breast tumor cells (MDA-MB-231 or SKBR-3), and in the presence or absence of JAK inhibitor or PI3K inhibitor. In these adipocytes, the expression of PLOD2 at mRNA level was measured by qPCR assay. c,d Analysis of phosphorylation (tyr705) STAT3, total STAT3 and PLOD2 protein expression was done using western blot analysis with extracts from mature adipocytes cultivated in the presence or in the absence of breast cancer cells (MDA-MB-231 or SKBR-3), and in the presence or absence of JAK inhibitor (ruxolitinib). e,f Analysis of phosphorylation (tyr705) STAT3, total STAT3 and PLOD2 protein expression was done using western blot analysis with extracts from mature adipocytes cultivated in the presence or in the absence of breast cancer cells (MDA-MB-231 or SKBR-3) in the presence or absence of PI3K inhibitor (LY294002). g,h Western blot analysis of phosphorylation (ser473) of AKT and total AKT of adipocytes in the presence or absence of breast cancer cells (MDA-MB-231(g) or SKBR-3(h)), which treated with tiplaxtinin in the cocultured system. i Analysis of phosphorylation (ser473) of AKT and total AKT of adipocytes in the presence or absence of PAI-1(200 ng/ml), which was treated with combination of LY294002