SLC25A3 (Solute Carrier Family 25 Member 3)

In contrast, under standard low-Cu conditions, CTR1 remains required for cellular Cu uptake and CuCOX metallation. Together, these findings define context-dependent Cu trafficking pathways in renal cancer and establish SEC-ICP-MS as a sensitive platform for assessing CuCOX metallation and mitochondrial metabolism, with potential applications in biomarker discovery and therapeutic targeting in RCC.

Ion channels and ecDNA are central to the disease progression and treatment resistance of PCa through regulation of EMT, CSC phenotype, and tumor microenvironment (TME) interactions. Targeting the drivers-through ion channel modulators, ferroptosis induction, and ecDNA-targeting interventions (BET/HDAC inhibitors, CRISPR-based methods) offers a promising way to overcome resistance. Integration of multi-omics, and combination treatments will be key to construct precision medicine strategies and improve clinical outcomes in advanced PCa.

Notably, we highlight the potential regulatory role of ANK2 in the progression of CRC. This research provides theoretical support and new directions for early screening, diagnostic biomarker identification, and targeted therapy strategies for CRC.

This study identifies SLC25A39 as a novel oncogenic driver in HCC. By stabilizing PRDX1 and sustaining mitochondrial redox balance, SLC25A39 promotes tumor progression while preventing necroptotic cell death. Targeting the interplay between SLC25A39, PRDX1, and necroptotic signaling may provide new therapeutic opportunities for HCC.

Thus, SLC35F4 and SLC35F5 but not closely related SLC35F3 likely import FAD into the Golgi apparatus, where the cofactor serves as the oxidant for disulfide-bond formation during tissue-specific, post-translational modification of secretory proteins. These findings provide strong direction for the definitive experiments yet needed to confirm the carriers' subcellular localization, transport activities, and contributions to protein maturation and trafficking.

Further multi-omics analysis revealed that the oncogenic effects of SLC25A3 in HCC may be mediated through its regulation of mitochondrial function and chromatin remodeling. These findings offer valuable insights for identifying potential therapeutic targets for HCC.

This study identified seven prognostic genes and provided a new theoretical basis for exploring immune defense mechanisms and targeted therapeutic drugs in PRAD.

It was stated that the AHR, EPHX1, GSTP1, and SLC25A32 did not correlate in healthy intestinal tissue whereas AHCY, ALDH1A1, NNMT, GSTM4, UGT2B17, and SLCO1B3 did not correlate in CRC. The disturbed transcriptional activity of genes related to the biotransformation process at all stages of CRC suggests that this may be the cause of its occurrence; the genes ought to be taken into account in preventive strategies and the treatment of patients.

Our study reveals SLC25A39 as a critical regulator of HCC progression via the mitochondrial ROS-cytochrome c-caspase signaling axis, highlighting its potential as a diagnostic biomarker and therapeutic target in HCC.

Mechanistically, circSHOC1 interacted with mitochondrial protein SLC25A3 (Solute Carrier Family 25 Member 3), a key oxidative stress regulator; SLC25A3 knockdown mitigated DNA damage (P < 0.01), and co-transfection experiments confirmed SLC25A3 as a critical mediator of circSHOC1-driven genotoxicity. Collectively, this work provides the first experimental evidence that 2-NA induces bronchial epithelial DNA damage via a circSHOC1-SLC25A3-ROS axis, supporting a novel mechanism for tobacco-associated lung carcinogenesis and highlighting 2-NA as a potential pulmonary carcinogen.

Rare-variant polygenic scores derived from discovery significantly predicted continuous (R2 = 0.146, p = 9.08 × 10-12) and binary traits (AUC = 0.548, OR = 0.99, p = 9.22 × 10-6) in replication. This first rare-variant GWAS of vitamin D in Middle Easterners identifies novel loci and pathways, underscores the contribution of ancestry-specific rare alleles, and supports integrating rare and common variants to guide precision management in high-burden populations.