GPX4 expression

Finally, the combined inhibition of Trx1 and GCL had a synergistic effect on CML cells in murine xenograft models. These findings offer crucial informationregarding the combined roles ofTrx1 and GCL in triggering ferroptosis in CML and suggestefficacioustherapeutic uses for these systems in this disease.

ROC analysis verified the predictive role of ACSL4 expression for DFS and OS, with an area under the curve (AUC) of 0.713 and 0.663. The present study demonstrates that ACSL4 and GPX4 may serve as valuable prognostic biomarkers for long-term survival, and play a key translational role in individualized therapy for patients with ESCC.

Surprisingly, BG11 significantly inhibited tumor proliferation in the MDA-MB-231 xenograft model without obvious toxicity. Based on the above findings, BG11 may be the candidate dual ferroptosis and apoptosis inducers for treating TNBC.

Finally, Mapk8, as a ferroptosis driver, was remarkably elevated in E. faecalis-infected Gsta4-deficient macrophages. These results suggest that Gsta4 inactivation blocks MIBE by eliminating macrophages, thereby attenuates E. faecalis-induced colitis and CRC.

In addition, epicatechin increased the expression of nuclear factor erythroid-2 related factor 2 (Nrf2) and hemeoxygenase-1 (HO-1). We therefore conclude that epicatechin protected EMB-induced liver injury by preventing ferroptosis through activating Nrf2.

ME promoted ferroptosis in HCT116 and LOVO cells, reversing ROS, lipid peroxidation and GSSG/GSH radio level. In general, the findings stated that the polysaccharides provided effects of inducing colon cancer ferroptosis, uncovering potential function of ME from maggot as a candidate compound.

High SLC2A1 expression is correlated with poor prognosis of patients with LUAD, and inhibiting SLC2A1 can induce ferroptosis and autophagy of LUAD cells, suggesting the potential of SLC2A1 as a target for LUAD diagnosis and treatment.

After clarifying the promotion effects of the cancer associated fibroblasts (CAFs) in chemoresistance, and leveraging our previous elucidation of the anti-inflammatory and ferroptosis-inducing ability of mangiferin, we synthesized mangiferin amphiphile (MMF) and developed a self-assembled carrier-free nanomedicine, named MP, through the self-assembly of MMF and the representative chemotherapeutic drug paclitaxel (PTX)...Furthermore, MP effectively suppressed glutathione peroxidase 4 (GPX4) expression to induce ferroptosis, mitigated the activation of IL-6/STAT3 pathway to deactivate CAFs within the inflammatory TME, and exhibited robust anti-cancer effects against PTX-resistant breast cancer both in vitro and in vivo. This mangiferin derivative represents a promising "all-in-one" nanocarrier for delivering chemotherapeutic drugs, offering a green, safe, and convenient self-assembled carrier-free nanomedicine to effectively overcome drug resistance.

This study utilizes a doxycycline inducible GPx4 overexpression model to test this hypothesis...Moreover, analysis of patient derived GBM cells reveal that cell growth rates, plating efficiency, and Young's modulus are all inversely proportional to GPx4 expression. Therefore, GPx4 appears to be a biophysical regulator of GBM cell growth that warrants further mechanistic investigation in its role in GBM progression.

In vivo experiments showed that Obacunone effectively inhibited tumor growth. Obacunone exhibits potential therapeutic significance through the modulation of the Akt/p53 signaling pathway, which may induce ferroptosis and inhibit the proliferation of ovarian cancer cells.

Our results suggest that PFKFB3 inhibition reduces glucose utilization and DNA damage repair, limiting the adaptivity of the cells to therapy-driven oxidative stress and DNA integrity insults. Inhibiting PFKFB3 can be an effective strategy to eradicate cancer cells surviving under EGFR TKI therapy before they enter the drug-resistant state. These findings may have potential implications in the development of new therapies for drug-resistant cancer treatment.

SHP2 advances CRC progression by modulating TFEB-mediated ferritinophagy, suppressing ROS and ferroptosis. Targeting SHP2 presents a promising therapeutic strategy for CRC.