In conclusion, our findings indicate that CL-387785 induces necroptosis in tumor cells via the TRADD/RIPK1/NF-κB/CD80 signaling pathway, thereby sensitizing tumors to anti-PD-1 therapy. These results suggest that CL-387785 is a promising candidate for increasing tumor immunotherapy efficacy.
Exo‑si‑PYCR1 blocked xenograft tumor growth and had good biocompatibility. Briefly, PYCR1 knocking loaded by BMSC‑derived Exos suppressed aerobic glycolysis and BC growth via the PI3K/AKT pathway by binding to EGFR.