NRF1 (Nuclear Respiratory Factor 1)

Regression analysis was conducted utilizing the parameters of PWG, GPT activity, and ATP content, and the dietary Cr3+ requirements of juvenile grass carp were 1.02, 1.55, and 1.54 mg/kg, respectively. Overall, this study provided new insights into the effects of Cr3+ on GLU metabolism of juvenile grass carp under hypoxia stress, offering a nutritional regulation strategy for improving the ability of fish to resist hypoxia stress.

In summary, we report 7 new BRAF fusions in PTC BRAF V600E-WT. Additional clinical research is needed to elucidate the behavior of BRAF fusion-driven thyroid carcinomas and the therapeutic utility of MAPK pathway inhibitors.

In this study, we revealed for the first time that FMD/fasting coordinates NRF1-UPS and Trex1/Sting-mediated type I interferon responses in TAMs that contribute to suppressing tumour growth. Graphical abstract: FMD upregulates the entry of NRF1 into the TAM nucleus to promote gene expression of proteasome subunits, which induces the ubiquitin/proteasome-dependent proteolysis of Trex1, leading to derepression of the cGAS-Sting-IFNβ axis. On the other hand, FMD triggers increasing of mtDNA in TAMs, promoting the cGAS-Sting-IFNβ axis to release IFNβ. In myeloid NRF1 knockout TAMs, transcriptional levels of proteasome subunits are reduced, resulting in impaired proteolysis of Trex1 and its subsequent accumulation during fasting. Then, Trex1 binds to mtDNA, directing the inhibition of the cGAS-Sting-IFNβ axis and inhibiting IFNβ secretion of macrophages.

Furthermore, neutralizing NRG1 enhanced the efficacy of sunitinib in RCC models in vivo. Together, these findings highlight targeting the tumor-promoting functions of ApoEhigh CAFs as a promising approach for treating advanced RCC.

Molecular docking highlighted Monomethyl lithospermate as a key active component. Overall, SLC influences oxidative phosphorylation via the PDK1/PDHA1 and SIRT1/PGC-1α/NRF1/TFAM signaling pathways and downregulates the HER2 pathway, thereby ultimately inhibiting HER2-positive breast cancer progression.

CEACAM1 regulates the PPAR signaling pathway key molecules, affecting OSCC cell autophagy, mitochondrial balance, and apoptosis.

Genetic ablation of GCN5 completely reversed γ-Elemene-induced PGC- 1α acetylation and restored mitochondrial biogenesis and cell viability, establishing a critical role for GCN5 in mediating these effects. Our findings reveal a novel mechanism whereby γ-Elemene disrupts mitochondrial function in TNBC through GCN5-mediated PGC-1α acetylation, providing new insights into its anti-cancer properties and potential therapeutic applications against TNBC.

The downregulation of prkaa1, encoding the catalytic subunit of AMP-activated protein kinase (AMPK), implicates disrupted metabolic adaptation and redox homeostasis as central features of IM-induced toxicity. Together, these findings suggest that IM provokes neurobehavioral disturbances in zebrafish through mitochondrial dysfunction, impaired AMPK signaling, oxidative stress, and secondary inhibition of AChE, ultimately leading to cholinergic dysregulation and anxiety-like responses.

In contrast, the overexpression of ATM or TFAM partially ameliorates the inhibition of tumor cell behavior and mitochondrial function induced by ultra-low background radiation. Collectively, these findings demonstrate that ultra-low background radiation inhibits tumor cell behavior through mitochondrial dysfunction mediated by ATM downregulation, providing valuable insights into the potential therapeutic applications and molecular targets of ultra-low background radiation.

Collectively, these insights identify IL-17 as a double-edged orchestrator whose context-dependent functions could be harnessed to surmount ICI resistance. Rationally designed, function-selective modulation of the IL-17 axis may unlock durable anti-tumour immunity for a wider spectrum of patients.

Rutin inhibits prostate cancer progression by suppressing EMT, inducing mitochondrial biogenesis, and acting via ER stress-linked AMPK/SIRT1 signaling. These findings suggest that Rutin may serve as a potential therapeutic candidate for advanced prostate cancer.

Among these, NR-CL was validated as a disulfidptosis desensitizer, while lomerizine and clioquinol were confirmed as sensitizers through gene expression predictive analyses and cellular functional validation. These findings lay a robust foundation for uncovering novel regulatory mechanisms of disulfidptosis and provide practical strategies for enhancing cancer chemotherapy through targeted interventions.