erastin

These findings may explain one of the reasons for the suboptimal efficacy of simvastatin in the treatment of pancreatic cancer, while also providing new insights for research on the antitumor effects of statins.

Moreover, USP18 silencing promoted the accumulation of lipid reactive oxygen species (ROS), malondialdehyde (MDA), and Fe2+, thereby enhancing erastin-induced ferroptosis...Subsequent rescue experiments confirmed that the tumor-promoting effects of USP18 were abrogated upon HDAC3 knockdown. Taken together, our results identify the USP18/HDAC3 axis as a key regulator of EC cell proliferation and ferroptosis suppression, underscoring the potential of USP18 as a therapeutic target in EC.

Our study successfully isolated SCRENs from Smilax china rhizomes and demonstrated their inhibitory effects on HCC cell proliferation, migration, and invasion through in vitro cellular experiments. Mechanistic investigations revealed that SCRENs mediate their anti-tumor effects primarily through modulation of mitophagy-associated ferroptosis via GPX4/ACSL4 axis.

SLC7A11 knockdown regulates intracellular redox balance through the GSH-GPX4 axis, thereby promoting cellular cuproptosis. Targeting SLC7A11 can enhance the sensitivity of CRC cells to copper ionophores and may represent a novel therapeutic strategy to enhance cuproptosis of CRC cells.

Ferrostatin-1 or Erastin successfully reversed the phenotype triggered by HSP27 alterations. HSP27 can induce the growth of CSCC by inhibiting ferroptosis, and is expected to become a new target for the treatment of CSCC.

Iron chelators and radical scavengers can stop it, while erastin or iron overload can cause it...These cell-based in vitro findings indicate that EGCG-rich GTE can attenuate ferroptosis-associated oxidative stress in hepatocytes under iron-loading conditions. GTE may serve as a potential dietary antioxidant candidate; further mechanistic studies and in vivo experiments are required to determine its physiological relevance and translational applicability.

Our research may provide intervention strategies for the treatment of OV.

KAT6A promotes the proliferation of CC cells and suppresses ferroptosis via epigenetic regulation of GPX4. Our work presented KAT6A as a potential diagnostic and therapeutic target for treatment CC.

Conversely, NSUN2 overexpression conferred ferroptosis resistance, reducing iron accumulation and restoring GPX4 expression even under erastin treatment...Notably, treatment with an autophagy inhibitor (3-MA) or a ferroptosis inhibitor (Fer-1) partially restored tumor growth in NSUN2-knockdown cells, validating the critical role of autophagy and ferroptosis in NSUN2-mediated OSCC progression. These findings identify the NSUN2-YBX1-SQSTM1/P62 axis as a key regulator of autophagy-dependent ferroptosis in OSCC, highlighting NSUN2 as a promising epitranscriptomic target to enhance ferroptosis induction for OSCC therapy.

A triple therapy combining CH-223191, ferroptosis inducer (Imidazole ketone erastin or RSL3), and anti-PD-1 agent demonstrates superior efficacy and safety in vivo. Together, our findings demonstrate that IL4I1⁺ TAMs and TDO2⁺ myCAFs synergistically establish an immunosuppressive, ferroptosis-resistant niche via AhR signaling in solid predominant LUAD and offer promising therapeutic strategies to reprogram the tumor microenvironment.

PS-MPs promote NPC progression by generating mitochondrial ROS that activate the NRF2-SLC7A11/GPX4 antioxidant axis and suppress ferroptosis. Pharmacologic reactivation of ferroptosis counteracts these effects, highlighting ferroptosis-targeted therapy as a potential strategy for mitigating microplastic-associated cancer risk.

However, mesenchymal-like bladder cancer cells exhibited heightened sensitivity to the ferroptosis inducer Erastin, showing more pronounced suppression of proliferation, elevated ROS, higher LPO and MDA levels, and reduced GSH, confirming their enhanced susceptibility to ferroptosis...In vivo experiments further demonstrated that targeting the Smad3/CISD2 axis significantly suppressed xenograft tumor growth and activated ferroptosis. In conclusion, this study elucidates a novel mechanism by which the Smad3/CISD2 axis dynamically regulates ferroptosis through redox homeostasis reprogramming during EMT, providing a potential therapeutic strategy for targeting the progression of MIBC.