Ovarian cancer (OVC) is one of the deadliest and most aggressive tumors in women, with an increasing incidence in recent years. Cuproptosis, a newly discovered type of programmed cell death, is caused by intracellular copper-mediated lipoylated protein aggregation and proteotoxic stress. However, the role of cuproptosis-related features in OVC remains elusive. The single-cell sequencing data from GSE154600 and bulk transcriptome data of 378 OVC patients from TCGA database. The RNA-seq and clinical data of 379 OVC patients in GSE140082 and 173 OV patients in GSE53963. The PROGENy score was calculated to assess tumor-associated pathways. Based on gene set enrichment analysis (GSEA) of the cuproptosis pathway, the single cells were divided into the cuproptosis^high and cuproptosis^low groups. The differentially expressed genes (DEGs) between the two groups were screened, and 47 prognosis-related genes were identified based on univariate cox regression analysis. Randomforest was used to construct a prognostic model. Immuno-infiltration analysis was performed using ssGSEA and xCell algorithms. In vitro and in vivo experiments were used for functional verification. Six major cell populations was identified, including fibroblast, T cell, myeloid, epithelial cell, endothelial cell, and B cell populations. The PROGENy score which revealed significant activation of the PI3K pathway in T and B cells, and activation of the TGF-β pathway in endothelial cells and fibroblasts. TIMM8B, COX8A, SSR4, HIGD2A, WASF2, PRDX5 and CLDN4 were selected to construct a prognostic model from the identified 47 prognosis-related genes. Furthermore, the cuproptosis^high and cuproptosis^low groups showed significant differences in the expression levels of the model genes, immune cell infiltration, and sensitivity to six potential drug candidates. The functional experiments showed that WASF2 is associated with cuproptotic resistance and promotes cancer cell proliferation and resistance to platinum, and its high expression is associated with poor prognosis of OVC patients. A clinically significant cuproptosis-related prognostic model was identified which can accurately predict the prognosis and immune characteristics of OVC patients. WASF2, one of the cuproptosis-related gene in the risk model, promotes the proliferation and platinum resistance of OVC cells, and leads poor prognosis.

Particulate matter 2.5 (PM_2.5) has adverse biological effects on major living organs in the body, including lungs. The complex composition of PM_2.5, including carbon black and heavy metals, cause toxic effects to the lung. Nonetheless, there exists considerable knowledge gaps regarding the impact of carbon black (CB) on environmental health and safety (EHS). Thus far, the synergistic effects of CB have not gained much attention in past decades. Here, we showed that combined exposure of CB and Cadmium (Cd) enhance the cytotoxicity by altering the state of cell membrane. Specially, CB caused cell membrane collapse and increased the permeability of cells, and remarkedly enhanced the metal Cd toxicity. Furthermore, upon pre-treatment sublethal-dose CB, the increased intracellular Cd brought about a significantly amount of lactate dehydrogenase (LDH) and high expression of metallothionein-1 (MT-1) in human lung epithelial cell line (BEAS-2B) cells, and ultimately resulted an increased cellular toxicity. The lung of mice exposed CBs and Cd presented remarkably inflammation than Cd alone. Mechanistic exploration deciphered that CB pre-treatment triggered cell damage via apoptosis due to Cd exposure. Collectively, our findings reveal a novel path for understanding the impact of CB on EHS with its synergistic effects, through which nanomaterials might exert detrimental effects on organisms.

Iron is essential for vital cellular processes, including DNA synthesis, repair, and proliferation, necessitating enhanced iron uptake and intracellular accumulation. Tumor cells, in particular, exhibit a pronounced elevation in iron uptake to sustain their continuous proliferation, migration and invasion. This elevated iron acquisition is facilitated predominantly through the upregulation of transferrin receptors, which are closely associated with tumorigenesis and tumor progression. Incorporating transferrin into drug delivery systems has been shown to enhance cytotoxic effects in drug-sensitive cancer cells, offering a potential method to surpass the limitations of current cancer therapies. Intracellular iron predominantly exists as ferritin heavy chain (FTH), ferritin light chain (FTL), and labile iron pool (LIP). The innovation of nanocarriers incorporating iron chelating agents has attracted considerable interest. Iron chelators such as Deferoxamine (DFO), Deferasirox (DFX), and Dp44mT have demonstrated significant promise in cancer treatment by inducing iron deficiency within tumor cells. This review explores recent advancements in nanotechnology aimed at targeting iron metabolism in cancer cells and discusses their potential applications in cancer treatment strategies.

Background. Dead end 1 (DND1) plays a vital role during oncogenesis and cancer progression by regulating the mRNA content via competitive combination with miRNA, but what function it exerts in prostate cancer has been unclear. The purpose of this paper is to explore the correlation between DND1 expression levels and clinical characteristics in prostate cancer (PCa) patients. Materials and Methods. To assess the expression of DND1 in tumor specimens compared with paired paracancerous tissues, the sample from 83 patients was analyzed by immunohistochemistry. The Cancer Genome Atlas (TCGA) database was used to verify our results. Subsequently, we statistically analyzed the relationship between DND1 expression and the clinical prognosis of PCa patients. Results. Compared with paracancerous tissues, DND1 has a higher expression level in prostate cancer. The overexpression of DND1 in protein level was significantly associated with the higher clinical stage ( ), ISUP grading group ( ), seminal vesicle invasion ( ), and PSA density ( ). Furthermore, the overexpression of DND1 indicates a poor clinical prognosis in prostate cancer patients. Conclusion. High-level expression of DND1 was associated with tumor progression and poor clinical prognosis. Hence, DND1 may become a potential prognostic biomarker for PCa.