Our results demonstrated the anticancer efficacy of Ova in NPC and its potential as a putative inhibitor of JAK2 and STAT3, which are essential in tumorigenesis of NPC.
In this study, EBV negative and positive cell lines, and the JAK2/STAT3 signal pathway inhibitor AG490 were used to illustrate the role of vIL-10 in NPC.
Our data indicated that OIP5 was highly expressed in NPC and promoted NPC progression by modulating JAK2/STAT3; our results shed light on utilizing OIP5 as a potential novel therapeutic target for the treatment of NPC.
However, there was no direct evidence that inactivation of the JAK2/STAT3 signaling pathway was involved in regulation of siTRIM24, these results suggested that TRIM24 has an important role in the growth of NPC.
Induction of LPLUNC1 overexpression inhibited NPC cell proliferation, induced NPC cell arrest, promoted NPC cell apoptosis even after IL-6 stimulation and inhibited the growth of implanted NPC tumors in vivo, which were associated with decreasing cyclin D1 and Bcl-2 expression and the Janus kinase 2 (JAK2)/Stat3 activation, but enhancing Bax and p21 expression.