Fig. 4: CPX decreases p-STAT3 (Tyr705) to promote proliferation inhibition in GC cells.
From: Ciclopirox drives growth arrest and autophagic cell death through STAT3 in gastric cancer cells
A The protein levels of p-STAT3 (Tyr705), STAT3, p-Src (Tyr416), Src, CDK4, and Cyclin D1 in GC cells pretreated with MG132 (MGC: 100 nM; AGS: 100 nM; SGC: 200 nM) for 24 h and then treated with CPX at different times. B The levels of p-STAT3 (Tyr705) in the nucleus and cytoplasm of GC cells treated with CPX (MGC: 10 µM; AGS: 10 µM; SGC: 40 µM) for 24 h. Representative images of p-STAT3 (Tyr705) and the ratio of nuclear to cytoplasmic fluorescence were shown (Scale bar, 25 µm). The protein levels of p-STAT3 (Tyr705) in the nucleus and cytoplasm of GC cells were analyzed by nuclear/cytosolic fractionation and Western blotting. Data were shown as mean ± SD (n = 3, ****P < 0.0001). C Western blotting analysis of p-STAT3 (Tyr705), STAT3, CDK4, and LC3 protein levels in STAT3Y705F cell lines treated with CPX for 24 h. D The proliferation of STAT3Y705F GC cells after being treated with CPX for 24 h was detected using an EdU Cell Proliferation kit with Alexa Fluor 488. EdU incorporation was quantified using ImageJ Plus software (Scale bar, 200 µm). Data were shown as mean ± SD (n = 3, *P < 0.05, **P < 0.01).
