TNFAIP3 overexpression

Moreover, the intra-articular injections of TNFAIP3-overexpressing SSCs further improved the subchondral trabecular bone remodeling of OA rats. Thus, we report that TNFAIP3 from SSCs contributed to the suppression on the subchondral osteoblast necroptosis, which suggest that necropotic subchondral osteoblasts in joints may be possible targets to treat OA by stem cell therapy.

TNFAIP3 exhibits inhibitory effects on apoptosis and promotes testosterone production in Leydig cells. The protective influence of TNFAIP3 on Leydig cells within an inflammatory microenvironment is likely mediated through by inhibiting the P38MAPK pathway and upregulating CEBPB expression.

We found that TNFAIP3 inhibited the TNF signaling pathway, which could inhibit cell migration and proliferation and contribute to apoptosis. Overall, these findings highlighted TNFAIP3 as a tumor suppressor gene in the regulation of the progression and metastatic potential of prostate cancer and that targeting TNFAIP3 by ZY-444 might be a promising strategy for prostate cancer treatment.

Finally, TNFAIP3 overexpression could overturn the effects of miR-4735-3p mimic on LSCC cellular activities. In conclusion, our results demonstrated that PAX5-induced LINC00467 facilitated LSCC progression by inhibiting miR-4735-3p to increase TNFAIP3 expression.

Our evidences suggest the promising potential of utilizing TNFAIP3 and NFκB as important reference indices for determining the prognostic outcome of CRC. Furthermore, we revealed that TNFAIP3 overexpression inhibited CRC cell proliferation, invasion, and migration.

EVs reduced the sensitivity of DLBCL model mice to rituximab via the miR‑125b‑5p/TNFAIP3 axis. The study findings indicate that the tumor‑derived EVs carrying miR‑125b‑5p can enter DLBCL cells and target TNFAIP3, thus reducing the sensitivity of DLBCL to rituximab, which may provide a novel therapeutic approach for DLBCL.