AI Networking Cookbook: Practical recipes for AI-assisted network automation and development
TL;DR
USP8-mediated stabilization of GPR37 may contribute to ferroptosis resistance and CRC progression, potentially involving NRF2/SLC7A11/GPX4 signaling.
In vivo, GPR39 knockdown significantly potentiated the antitumor activity of PD‐1 blockade, as evidenced by suppressed tumor progression accompanied by enhanced infiltration of CD8+ T cells, whereas ferroptosis inhibition abrogated these effects.
USP7 suppresses ferroptosis and enhances growth in NSCLC cells by stabilizing SETDB1 protein through deubiquitination, and Mechanistically, USP7 enhanced the stability of SETDB1 protein by its deubiquitination.
Clinically, these findings identify the METTL1/USP48/LCN2 pathway as a potential therapeutic target for cSCC and elucidated a novel oncogenic axis in cSCC, wherein METTL1 stabilized USP48 mRNA through m7G methylation modification, and USP48 in turn deubiquitinated and stabilized LCN2 protein.
Multi-dimensional experiments reveal BA may regulate ferroptosis via the potential STAT3/HO-1/GPX4 signaling axis and is a promising therapeutic alternative to conventional chemotherapy, which is limited by severe systemic toxicity.
Functional experiments demonstrate that UBE2S promotes KIRC cell proliferation and migration while inhibiting apoptosis and drives KIRC progression by regulating CDC20 expression and suppressing FDX1‐mediated cuproptosis, thereby promoting tumor‐associated macrophage polarization.
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