ACSL4 (Acyl-CoA Synthetase Long Chain Family Member 4)

Cisplatin (DDP) is the first-in-class drug for advanced and non-targetable non-small-cell lung cancer (NSCLC). However, the effects were reversed by ferroptosis inhibitor ferrostatin-1 or deferoxamine in NSCLC cells. In summary, these results provide in vitro experimental evidence that PEM boosts the antitumor activity and increases the sensitivity of NSCLC cells to DDP by inducing ferroptosis.

Repurposed drugs such as flubendazole and the ezetimibe derivative L14-8, along with natural compounds including evodiamine and luteolin, demonstrate translational potential for ferroptosis induction. Collectively, ferroptosis represents a promising therapeutic vulnerability for precision treatment of advanced prostate cancer.

This study found that HSF4 overexpression markedly attenuated Erastin-induced cell death and mitochondrial damage in HT29 and HCT116 cells...In vivo experiments, MBOAT1/2 knockdown effectively reduced tumor volume and downregulated the number of Ki-67-positive cells, GPX4, and SLC7A11, while upregulating ACSL4. In conclusion, HSF4 alleviates ferroptosis in CRC cells and facilitates tumor progression by upregulating MBOAT1/2 transcription, thereby limiting lipid peroxidation and Fe2+ accumulation.

In conclusion, our findings reveal for the first time that the TG combined with DDP reverses EOC drug resistance through the simultaneous induction of ferroptosis (HIF-1α/ACSL4 and Keap1/Nrf2/ARE) and apoptosis (p53/Bax/Bcl-2). These results provide experimental evidence supporting the clinical application of TG in overcoming DDP chemotherapy resistance in EOC.

Erianin induces ferroptosis via PDP2-mediated activation of the JNK signaling pathway, thereby restraining ovarian cancer growth in vitro and in vivo. These findings provide a mechanistic rationale for further evaluation of Erianin as a ferroptosis-inducing therapeutic candidate, including in chemoresistant settings.

Histopathologic evaluation revealed characteristic features of invasive melanoma, including atypical melanocytic nests, pagetoid spread, cytologic atypia, and architectural disorder. Overall, ACSL4 expression was significantly upregulated in primary cutaneous melanoma compared with normal skin, particularly within dermal atypical melanocytic tumor cells, suggesting that ACSL4 may contribute to melanoma biology through lipid metabolic pathways and may represent a potential biomarker of tumor aggressiveness, warranting further investigation into its diagnostic and prognostic relevance.

In addition, the ferroptosis inducers erastin and RSL3 are capable of enhancing the efficacy of traditional therapies and seeking solutions for the chemoresistance problem. The hurdles to be overcome are finding reliable biomarkers for the prediction of ferroptosis sensitivity and designing targeted delivery systems for minimal off-target effects. Clinically, these techniques offer novel concepts in the treatment of CCA, making further research key to these conclusions being adopted in practice.

Importantly, ferroptosis induction promotes immunogenic cell death, enhancing T cell infiltration and synergizing with immune checkpoint blockade to achieve sustained antitumor immunity. This review delineates the molecular basis of ferroptosis sensitivity in resistant cancers, explores immune-ferroptosis crosstalk, evaluates combination strategies with immunotherapy, and discusses challenges such as toxicity and patient stratification to advance clinical translation.

Other clinicopathological factors, including tumor grade, stage, size, and receptor status, were not significantly related to metastasis. Our study highlights the importance of HER-2 as a key prognostic marker in breast cancer and suggests that further research is required to clarify the mechanisms underlying its role in cancer progression.

Silencing SP1 significantly attenuates trastuzumab-triggered myocardial ferroptosis. Collectively, our findings establish ferroptosis as the primary pathway underlying trastuzumab-associated cardiotoxicity and propose SP1 inhibition as a promising therapeutic strategy to mitigate this adverse effect.

Papain exhibits antileukemic effects in vitro, associated with mitochondrial-mediated apoptosis, altering cell-cycle progression, suppressing Sema3A expression, and modulating inflammatory responses. These findings suggest that papain may represent a candidate for further preclinical investigation in leukemia models.

As the nuclear translocation of RB1CC1 was promoted by the JNK signaling pathway, SP600125, a JNK inhibitor, prevented the MPD-induced RB1CC1 nuclear translocation. In summary, MPD induced the dissociation of RB1CC1 from DRMs and its subsequent nuclear translocation, contributing to ferroptosis of prostate cancer cells.