Journal of Cancer Prevention

eISSN 2288-3657
pISSN 2288-3649
Fig. 3.

Download original image

Fig. 3. 15d-PGJ2-mediated inactivation of STAT3 through inhibition of STAT3 dimerization. (A, B) Whole extracts were prepared and examined by immunoblotting for P-STAT3Y705, STAT3 and β-actin in MDA-MB-231 and MDA-MB-468 cells. (C) LNCaP prostate cancer cells were pre-incubated in 15d-PGJ2 (5, 10, 30 μM) for 5 hours and treated in interleukin-6 (IL-6) (10 ng/mL) for 16 hours. Whole extracts were prepared and examined for P-STAT3Y705, STAT3, cyclin D1 and β-actin by immunoblot analysis. (D) Luciferase activity was measured with LNCaP cells preincubated with indicated concentrations of 15d-PGJ2 for 5 hours and then stimulated with IL-6 for 16 hours. **P < 0.01; ***P < 0.001. (E) PC-3 cells were co-transfected with HA-tagged STAT3 and Myc-tagged STAT3 and treated with 15d-PGJ2 for 24 hours. The total lysates obtained from the transfected cells were immunoprecipitated with anti-HA antibody and analyzed by Western blotting with anti-Myc or anti-HA antibody. 15d-PGJ2, 15-deoxy-Δ12,14-prostaglandin J2; P-STAT3, phosphorylated form of STAT3; IL-6, interleukin-6; IP, immunoprecipitation; HA, hemagglutinin; IB, immunoblotting.
J Cancer Prev 2021;26:207~217
© J Cancer Prev
Copyright © Korean Society of Cancer Prevention. / Powered by INFOrang Co., Ltd