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. 2016 Dec 20;8(7):10954–10965. doi: 10.18632/oncotarget.14032

Figure 6. The influence of LMP1-IgG on the JAK/STAT pathway in ENKTL.

Figure 6

(A) Phosphorylation of STAT3 was substantially inhibited after LMP1-IgG treatment in SNK6 cells in a concentration- and time-dependent manner. In contrast, phosphorylation of STAT5 was rarely changed. (B) Detection of activation (phosphorylation) levels of the relevant tyrosine kinases in the Janus family (JAKs). LMP1-IgG inhibited the phosphorylation of JAK3 in a dose- and time-dependent manner, but rarely influenced that of JAK1, JAK2 and TYK2. (C) Two LMP1-siRNAs and a control-scrambled siRNA were constructed, and LMP1 expression in SNK6 cells was successfully inhibited. LMP1-siRNA2 showed better inhibitory effectiveness for LMP1 expression and was chosen for subsequent experiments. (D) and (E) LMP1 expression knockdown attenuated the inhibition of phosphorylation of JAK3 and STAT3 (SNK6-LMP1Si). In comparison, significant inhibition of phosphorylation of JAK3 and STAT3 was apparent in the control siRNA group (SNK6-LMP1Scr).