To summarize, these findings demonstrate that Ten effectively inhibits lung cancer and activates immunocytes by KDM5B inhibition, which is regulated by TEX264-associated ER-phagy. Most importantly, OTUD3 serves as an essential target for enhancement of TEX264 stabilization.
These findings suggest that Teniposide activates STING through a previously unrecognized, cGAS-independent mechanism, while retaining potential for canonical cGAS-STING stimulation. Our combined computational and experimental evidence supports repurposing Teniposide as a STING agonist, highlighting new therapeutic possibilities for innate immune stimulation.
As of June 2025, the patient has achieved a CR with a progression-free survival of 9 months before experiencing disease recurrence. This rare case of NF1-associated oligodendroglioma was managed with thiotepa, bevacizumab, teniposide, and tunlametinib, highlighting the potential of MEK inhibition in NF1-related gliomas.
This study provides compelling evidence supporting the potential therapeutic significance of inducing MC-mediated apoptosis in OSCC. The results underscore the role of PPT and its derivatives, such as etoposide and teniposide, in targeting rapidly dividing cancer cells through interference with mitotic progression, offering insights into novel therapeutic strategies for oral cancer.
In summary, these data make a strong argument for the notion that Ten/VM-26-mediated inhibition of APEX1 contributes to DNA damage and thereby achieves favorable antilung cancer effects, wherein Ten/VM-26 could down-regulate APEX1 by binding and ubiquitination. The current study presents a critical target and mechanism for Ten/VM-26-mediated antilung cancer therapy.