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Fig. 6 | Journal of Experimental & Clinical Cancer Research

Fig. 6

From: Combination therapy with protein kinase inhibitor H89 and Tetrandrine elicits enhanced synergistic antitumor efficacy

Fig. 6

c-Myc sensitizes cancer cells to H89/tetrandrine combination treatment. a Western blot of c-Myc in H89/tetrandrine sensitive cells (MDA-MB-231, AGS, LOVO and Hep3B) and resistant cells (Huh7, A549, HCCLM9 and HCT116). b HCT116 and A549 cells engineered to overexpress c-Myc and exposed to H89/tetrandrine combined treatment. Cell viabilities and PARP activation were determined at 72 h and 48 h, respectively. c Apoptosis was detected by flow cytometry in HCT116 c-Myc overexpressing cells after H89/tetrandrine combination treatment for 48 h. d AGS and MDA-MB-231 cells were stably transduced with lentiviral vectors that expressed c-Myc shRNAs (#1 or #2) and negative control vector PLKO.1 (shCtrl); c-Myc protein levels were subsequently detected to confirm the knockdown efficiency. e shRNA mediates c-Myc knockdown in AGS and MDA-MB-231 cells undergoing H89/tetrandrine combination treatment. Cell viabilities and PARP were determined as previously described. f MDA-MB-231 knockdown of c-Myc following treatment with H89/tetrandrine for 48 h. Apoptosis was detected by Annexin V/PI staining. g c-Myc and Mcl-1 levels were determined by Western blot in AGS and MDA-MB-231 cells after knockdown of c-Myc and HCT116, A549 cells overexpressing c-Myc. h Western blot of LC3 in AGS and MDA-MB-231 c-Myc knockdown cells following H89/tetrandrine combination treatment for 24 h. i AGS and MDA-MB-231 cells were transduced with c-Myc shRNA#1 or shCtrl. Intracellular ROS were determined by flow cytometry after H89/tetrandrine treatment for 24 h. Data are reported as the mean ± SD and were analyzed by Student’s t-test; all data represent at least n = 3 independent experiments; *P < 0.05, **P < 0.01. All images are representative of at least three independent experiments

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