Fig. 6

CM from M1-like TAMs regulated the malignant behaviors of OSCC cells via the JAK/STAT3 pathway. A. OSCCs cells were lysed after treatment with CM from M1-like TAMs or M0 for 6h, and the activation status of cellular signaling was detected by using Human Phospho-kinase Array Kit. A significant activation of the p-Stat3 (Y705) was detected in the SCC25 and Cal27 cells treated with CM from M1-like TAMs; B. The activation of Stat3 was validated by immunofluorescence in SCC25 and Cal27 cells treated with CM from M1-like TAMs (400x); C. The activation of Stat3 was validated by WB in SCC25 and Cal27 cells treated with CM from M1-like TAMs in a time-dependent manner; D. IL6-Ab blocked the activation of Stat3 in SCC25 and Cal27 cells treated with CM from M1-like TAMs; E. The activation of Stat3 in SCC25 and Cal27 cells were blocked under the treatment with CM from M1-like TAMs and Ruxolitinib (50nM). F-I. Ruxolitinib (50nM) reduced the effects of CM from M1-like TAMs on the colony formation (F), microsphere forming (G), migration (H), and invasion (I) potential of SCC25 and Cal27 cells. Data were represented as the mean ± SD of three independent experiments, **p<0.01