Figure 2
From: Role of MAPK in oncolytic herpes viral therapy in triple-negative breast cancer
(a) NV1066 downregulates the MEK/MAPK pathway in TNBC in vitro. Immunoblotting of MAPK pre and post viral treatment in five TNBC cell lines. Both phosphorylated and non-phosphorylated MAPK are shown. Actin is shown as loading control. Time of collection of cell lysates after infection is shown in hours. (b) NV1066 has no significant effects on PI3K and mTOR signaling pathway in TNBC in vitro. Immunoblotting of Akt and S6 pre and post viral treatment with NV1066 in 2 TNBC cell lines, HCC1837 and HCC38. Both phosphorylated and non-phosphorylated Akt and S6 are shown as components of PI3K/mTOR signaling pathway. Actin is shown as loading control. Time of collection of cell lysates after infection is shown in hours. (c) Baseline expression of p-MAPK in TNBC cell lines. Western blotting of phosphorylated and total MAPK expression from lysates from non-treated TNBC cell lines. Twenty microgram of protein was loaded per well. Cell lines MDA-MB-231, HCC1806 and HCC38 showed higher baseline expression of p-MAPK compared with HCC1937 and HCC1143. Higher expression level of p-MAPK correlated with increased sensitivity to viral oncolysis (indicated by increasing arrow sign). Actin antibody was used for equal loading.
