erastin

Ferroptosis was induced in B-ALL cells using erastin...PRDX1 knockdown further reduced the viability of B-ALL cells treated with the ferroptosis activator ML210, and treatment with the ferroptosis inhibitor liproxstatin-1 significantly reversed the suppressive effect of PRDX1 knockdown on xenograft tumor growth. Mechanically, PRDX1 deletion triggered ferroptosis in B-ALL cells by inhibiting the cAMP pathway. PRDX1 deficiency modulates ferroptosis in B-ALL cells by blocking the cAMP pathway, which offer a novel perspective on the pathogenesis of B-ALL.

The CHPT1-pSTAT3-SLC7A11 axis governs ferroptosis-dependent chemoresistance in PDAC. Dual targeting of CHPT1 and ferroptosis pathways represents a promising strategy to overcome GEM resistance, highlighting metabolic-kinase crosstalk as a therapeutic vulnerability.

The ferroptosis inducer erastin also inhibits melanoma growth. Combining the ATAD2 inhibitor BAY-850 with the MEK inhibitor trametinib potently suppresses melanoma growth. Our study identifies ATAD2 as a key driver of melanoma and provides a rationale for targeting ATAD2 in conjunction with the MAPK pathway to treat melanoma.

In the autophagy mediated by copper and erastin (a ferroptosis inducer), the autophagy receptors TAX1BP1 and SQSTM1 can promote the degradation of GPX4, effectively reducing the resistance of cancer cells to ferroptosis...In this review, we conduct a comprehensive and in-depth analysis of the roles played by selenoproteins derived from selenium metabolism in the regulation of immune cells associated with immune diseases. Moreover, we elaborate in detail on the effects of GPX4 in relation to ferroptosis in solid tumors under the influence of autophagy-mediated immunomodulation.

The HCC cells HepG2 and SNU449 were treated with five drugs, namely, dimethyl sulfoxide, AZ-628, SU-5402, TG-101209, and SPP-86, combined with donafenib to determine half-maximal inhibitory concentration values...Ferrous ion (Fe2+) and reactive oxygen species levels were measured after Erastin/RSL3 induction...In vivo experiments demonstrated a combined anti-tumor efficacy of AZ-628 and donafenib in HCC models (P < 0.0001). The findings of this study reveal a new combination therapy targeting the TK pathway for the treatment of HCC and provide a theoretical foundation for addressing donafenib resistance.

Moreover, SLC7A11 inhibitors, particularly sulfasalazine and erastin, effectively reversed resistance, in 18 clinical trials (Phase I-III) completed over the last decade. Targeting SLC7A11 presents a promising therapeutic strategy to modulate redox balance, metabolism, and ferroptosis, towards efficient cancer treatments.

Knockdown of GPX4 by RNAi reversed the resistance of PTEN-deficient PC3 and LNCaP cells to Erastin. Collectively, our findings suggest that ferroptosis can serve as a potential therapeutic strategy for prostate cancer, and PTEN status may influence cellular sensitivity to ferroptosis.

This study highlights the potential role of PPIA as a critical oncogenic driver in liver cancer, suggesting that targeting PPIA could offer therapeutic advantages in the treatment of this malignancy.

Our results suggest that LEF1 inhibits ferroptosis in CRC cells by promoting SLC7A11 transcription, potentially serving as a therapeutic target for CRC. This study reveals that the promotion of CRC by LEF1 is associated with activating SLC7A11 transcription and inhibiting cellular ferroptosis, providing a new direction for clinical targeted therapy of CRC.

In addition, DpdtpA treatment also caused depletion of Gpx4 and xCT, triggering ferroptosis as Erastin acted...In addition, PI3K/AKT/mTOR/pathway was showed involving EMT and ferroptosis regulation. In short, our data suggested that the status of EMT and ferroptosis largely was dominated by the continuous NCOA4-mediated ROS production.

In addition, GNB2 over-expression increased the expression of heat-shock-protein family A(HSP70) member 5 (HSPA5) and the expression of glutathione peroxidase 4 (GPX4), which inhibited the cell death induced from Erastin...Restored expression of HSPA5 in BRCA cells with GNB2 knockdown rescued the effects. Therefore, the current study verifies GNB2 as an important driver in BRCA progression by up-regulating HSPA5/GPX4 and inhibiting ferroptosis, which highlights its potential role in the clinical diagnosis and treatment of BRCA.

Co-treatment with Tat-beclin 1 and erastin enhanced BECN1-SLC7A11 complex formation, more strongly inhibited system Xc⁻, enhanced lipid peroxidation, inhibited the Nrf2-Keap1 signaling pathway and significantly suppressed tumor growth in vivo. Tat-beclin 1 promotes ferroptosis and tumor suppression in NSCLC by activating BECN1 and inhibiting SLC7A11-mediated system Xc⁻ activity.