ACO1 (Aconitase 1)

Moreover, 6-OHDA induces distinct inflammatory responses depending on the stage of oligodendrocyte differentiation. These findings highlight the dual role of oligodendrocytes as both iron reservoirs and modulators of the neuroinflammatory microenvironment, providing new insights into the cellular mechanisms underlying nigral iron accumulation in PD, and suggesting that oligodendrocytes play a critical regulatory role in PD pathogenesis.

The review shows that NFS1 plays an important role in cellular fate regulation, which has significant clinical application potential in the treatment of cancer and interventions for neurological and cardiovascular diseases. Therefore, it can provide a new theoretical basis and research direction for subsequent mechanism research and targeted therapeutic strategy development.

Moreover, we identified five potential conformational targets, including ACLY, ACO1, ACO2, IDH1, and OGDH, which may provide valuable insights into the molecular pathways underlying gemcitabine resistance in pancreatic cancer. Overall, these results offer insights into protein conformational changes and their potential link to phosphorylation in the context of cancer-stromal cell interactions, paving the way for structure-based, targeted therapeutic strategies for pancreatic cancer treatment.

Correlation analysis of DepMap gene-dependency profiles revealed distinct vulnerability patterns associated with non-canonical TCA cycle activity, outlining a characteristic landscape of genetic dependencies. Together, our integrative framework uniting constraint-based metabolic modeling and machine learning systematically reveals how non-canonical TCA cycle dynamics underpin metabolic plasticity and promote malignant traits.

The influence of G228A and G250A substitutions on G4 stability under physiological conditions was investigated. It was established that the low-molecular weight ligands BRACO19 and TMPyP4, the well-studied stabilizers of the G4 structure, can effectively interact with the hTERT promotor central G4 in the range of concentrations 5-25 μM.

ID is closely associated with aggressive tumor biology, suboptimal response to neoadjuvant therapy, and impaired postoperative recovery. Dysregulation of iron homeostasis and ferroptosis pathways in ID patients may contribute to CRC progression. These findings highlight ID as a potential biomarker for risk stratification and suggest that targeting iron metabolism could improve therapeutic outcomes in CRC management.

TIA1 gene, stress granule (SG) marker, is tightly regulated by miR-33a/KDM5C/H3K4me3 axis and exosomal miR-33a diminishes the formation of stromal SGs in CAFs. Collectively, our study reveals tumour selectively secretes miR-33a-5p through EVs to remodel the stromal SG formation and gain survival possibility for cancer cells in tumour core region, highlighting a novel regulatory mechanism of iron and nutrient level on EV secretion and the function of polyamine metabolism in reshaping epigenetic profiles.

siRNA-mediated ENO1-targeted knockdown would upregulate the mitochondrial iron transport channel through the ENO1-IRP1-Mfrn1 pathway, which subsequently leads to mitochondrial iron overload and the increase of detrimental mitochondrial reactive oxygen species (ROS), thereby triggering severe mitochondria destruction and causing mass death of tumor cells. Noteworthily, it is found that cRGD-VFs-mediated mitochondrial iron overload can activate powerful antitumor immunity by upregulating immune-related pathways to eliminate tumors, achieving notable tumor suppression in multiple murine liver cancer models, which represents a promising strategy of disturbing mitochondrial iron homeostasis for potentiating antitumor immunotherapy.

IRP1, APOA2, IGF1, A1BG, and SLC27A5 were up-regulated in matcha tea groups compared to control while, SLC27A5 was down-regulated in chia groups and Leptin and GRP78 were showed down-regulated in chia and matcha groups. This study offers new insights into the role of chia seeds and matcha tea in physiological and biological processes in the liver and achieved a vital and healthy biological body and reduces the incidence of cancer.

Moreover, the change in TACO1 expression affected multiple immunological components to regulate the generation of an immunosuppressive tumor microenvironment (TME). In conclusion, we first report on the role of TACO1 in gastric cancer, with findings suggesting that TACO1 could represent a promising prognostic and immunological biomarker for gastric cancer.

Cultured astrocytes treated with hydrogen peroxide over-released glutamate via xCT. These observations provide in vivo and in vitro evidence that microglia and astrocytes are glutamate suppliers in response to soluble iron overload and oxidative stress, respectively, in sporadic ALS.

All five genes were significantly downregulated in ccRCC tumors and mouse xenograft tumors. The results from this research demonstrate the oncogenic ability of miR-2355-5p and shed light on the possible mechanism by which this miRNA controls angiogenesis and tumor growth in VHL-deficient ccRCC.