erastin

Using rat spinal cord neurons in vitro, we found that erastin increased levels of Fe2+, RIG-I, and CCL5, effects that were reversed by the iron chelator deferoxamine. Intrathecal administration of deferoxamine or RIG-I siRNA attenuated pain behaviors and downregulated the expression of both RIG-I and CCL5. These findings demonstrate the spinal Fe2+/RIG-I/CCL5 pathway as a critical promoter of BCP and highlight the potential therapeutic strategies targeting iron chelation or RIG-I signaling.

Our findings reveal a novel miR-214-3p/GPX4/ferroptosis axis in OSCC DDP resistance. miR-214-3p suppresses GPX4 to promote ferroptosis, thereby reversing DDP resistance. This study identifies miR-214-3p as a potential therapeutic target for overcoming chemoresistance in OSCC by modulating ferroptosis.

Our studies might offer insights for the application of ferroptosis or macrophage polarization in the therapy of OSCC.

Significantly, Erastin-a SLC7A11 inhibitor-overcame YBX1-mediated resistance, synergizing with 5-Fu to induce ferroptosis and suppress tumor growth. Collectively, we unveil the ODC1-YBX1-SLC7A11-ferroptosis axis as a central mechanism of chemoresistance in STAD. Targeting this axis-via ODC1 inhibition or ferroptosis induction-represents a novel therapeutic strategy to reverse treatment resistance in gastric adenocarcinoma.

Lipophagy can promote RAS-selective lethal 3 (RSL3)-induced ferroptosis. LAPTM5 enhanced the sensitivity of glioma cells to ferroptosis inducer erastin, while suppression of lipophagy inhibited LAPTM5-mediated sensitization to erastin. The finding that glioma cells with high LAPTM5 expression were more sensitive to ferroptosis inducers suggests that glioma patients with high LAPTM5 expression may be more responsive to ferroptosis-inducing therapies.

Here, we identify EBV latent membrane protein 1 (LMP1), a key viral oncogene necessary for B cell immortalization and which mimics aspects of CD40 signaling, drives resistance to ferroptosis induction by erastin, a small molecule that blocks cystine uptake...PFKFB4 was also necessary for LMP1-mediated Burkitt B cell ferroptosis resistance. Collectively, these results identify PFKFB4 as a key host cell EBV metabolism remodeling target critical for infected B cell redox defense.

However, PRDX4 overexpression showed opposite effects, which were partly reversed by the ferroptosis inhibitor, ferrostatin-1 and the inducer erastin. Most crucially, PRDX4 depletion-mediated inactivation of the phosphoinositide 3-kinase (PI3K)/AKT signaling pathway could be rescued by 740 Y-P (a PI3K activator), whereas PRDX4 overexpression triggered the activation of the PI3K/AKT signaling pathway, which could be reversed by the PI3K inhibitor LY294002. Collectively, the data suggest that PRXD4 suppresses ferroptosis in ESCC cells by activating the PI3K/AKT signaling pathway, suggesting that targeting PRDX4 may be a novel strategy for treating patients with ESCC.

Clinically, genetic silencing of UBE2C induces ferroptosis and sensitizes tumor cells to the ferroptosis inducer erastin, revealing a therapeutically exploitable vulnerability in MYCN-amplified malignancies. Our study reveals a previously unrecognized MYCN-UBE2C-TFRC-ferroptosis regulatory axis that drives neuroectodermal tumor growth. These findings establish a mechanistic rationale for combining UBE2C silencing and ferroptosis induction as a precision therapeutic strategy against MYCN-amplified tumors.

The study demonstrated that COL11A1 exerts its oncogenic effects by suppressing autophagy via the AKT/Beclin 1 pathway, consequently inhibiting ferroptosis in pancreatic cancer cells. These findings reveal a novel molecular mechanism through which COL11A1 promotes tumor progression and provide a potential therapeutic target for pancreatic cancer treatment.

TRIM31 promotes ESCC progression by degrading VDAC1 and suppressing ferroptosis. Targeting TRIM31 enhances ferroptosis-based therapy and represents a novel, clinically actionable strategy for ESCC treatment. Antioxid. Redox Signal. 44, 550-571.

The effects of NUPR1 knockdown on GSH, ROS, lipid peroxidation, iron, and MDA levels were comparable to those observed after erastin treatment...Notably, the effects of NUPR1 overexpression were partially reversed by the LCN2 knockdown. These findings suggest a significant association between NUPR1 and LCN2, indicating that NUPR1 may serve as a potential therapeutic target for CRC treatment.

We also demonstrated that chemical inhibition of these proteins using RSL3 (GPX4 inhibitor) and erastin (xCT inhibitor) significantly suppressed osteosarcoma cell growth. Collectively, our findings reveal that GPX4 inhibition initiates ferroptosis while simultaneously activating NRF2-driven antioxidant defenses, iron homeostasis mechanisms, and adaptive cell survival signaling. The results highlight potential therapeutic strategies that combine GPX4 inhibition with targeted disruption of compensatory pathways to overcome ferroptosis resistance in osteosarcoma.