HSPB1 (Heat shock 27kDa protein 1)

Comprehensive in vivo evaluations confirmed the multidimensional chemosensitizing efficacy of MH alongside favorable biosafety. Our findings highlight MH as a promising adjuvant strategy for pancreatic cancer, particularly in GEM-resistant cases, by overcoming chemoresistance through the potentiation of ferroptosis.

Targeting HSPB1 exerts dual anti-tumor effects: it directly suppresses neoplastic proliferation and simultaneously alleviates Treg-mediated immunosuppression within the tumor microenvironment.

Our findings further revealed previously uncharacterized somatic copy number alterations, extrachromosomal DNA landscape, and human-HPV fusion peptides, with implications for genetic heterogeneity and therapeutic targets. This study enhances the understanding of cervical cancer through deeper proteogenomic insights, and facilitates the development of personalized therapeutic strategies to improve patient outcomes.

These findings identify a previously unrecognized function of PFKFB4 in GC, extending beyond its canonical metabolic roles to include active regulation of ferroptosis, thereby promoting cancer progression. Consequently, pharmacological inhibition of PFKFB4 represents a promising therapeutic avenue for overcoming ferroptosis resistance and suppressing tumor progression in gastric cancer.

An apoptosis-related gene prognostic model (AS model) with high predictive performance was constructed and had close associations with the tumor immune microenvironment and intercellular communication. The HSPB1 had a good predictive effect on GBM prognosis.

This pan-cancer resource links ferroptosis-related genes to survival outcomes and highlights SLC7A11, BECN1, and GLS2 as high-priority candidates for future mechanistic and clinical studies. Integrating sex as a biological variable into study design and interpretation will enhance clinical relevance.

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.

Utilizing a panoptosis gene set, this study identified eight core genes involved in hepatic IRI, providing novel insights into panoptosis' role in hepatic IRI.

Overexpression of Alkbh5 increased Hspb1 expression and inhibited ferroptosis, indicating that Alkbh5 regulates ferroptosis through targeting Hspb1. Targeting Alkbh5/Hspb1/ferroptosis axis may enhance anti-tumor effects in combination therapy, highlighting a potential therapeutic approach for HCC.

Current therapies include platinum, Taxol, angiogenesis inhibitors, and poly[ADP-ribose]polymerase (PARP) inhibitors...In contrast, expressing exogenous HSPB1 partially rescues the cell proliferation in ZKSCAN3 knockdown cells, which supports HSPB1 as a functional target gene of ZKSCAN3. Collectively, our study uncovers a functional ZKSCAN3-HSPB1 axis that promotes ovarian cancer cell proliferation.

Our study revealed that inflammation might exacerbate astrocyte ferroptosis. Additionally, NEAT1, HSPB1, and HSPA5 might serve as diagnostic markers for ferroptosis in PD.