ACACA (Acetyl-CoA Carboxylase Alpha)

Conclusion Both extrinsic factors (tumor-associated bacterial communities, tumor immune contexture and air pollution) and intrinsic factors predict EC recurrence. The complexity of tumor and host factors influencing cancer relapses underscore the need for more individualized prediction models of disease outcomes.

Furthermore, PS reduced hepatic pro-inflammatory cytokine mRNA levels: tumor necrosis factor α(tnf-α), cyclooxygenase 2 (cox-2), and interleukins (il-6, il-1β). In conclusion, dietary inclusion of 0.006%-0.018% PS effectively enhanced growth and antioxidant capacity, altered lipid handling, and affected transcriptional inflammatory responses.

The shortened tail and increased fat accumulation represent key adaptations for thermoregulation and energy conservation in high-latitude habitats. Notably, all Tibetan macaque populations experienced long-term selection pressures from cold at high latitudes, which have not only shaped distinctive adaptive traits, but may also render the species particularly vulnerable to contemporary climate warming, particularly for the eastern populations.

In vitro and xenograft experiments further demonstrated that ACACA promoted proliferation and migration and suppressed apoptosis, accompanied by reduced R-loop accumulation, enhanced fatty acid metabolism and improved mitochondrial function. Together, these findings identify ACACA as an R-loop-associated metabolic driver connecting genomic stress with lipid reprogramming and TME remodeling in ccRCC, supporting its potential as a prognostic biomarker and therapeutic target.

Our findings demonstrate a key SAM-independent link between methionine metabolism and mRNA m6A modification that affects demethylase substrate specificity. This novel link between the methionine cycle and lipid metabolism suggests new strategies for anticancer therapy.

An 18-month HFD successfully established a translational M. fascicularis model replicating key metabolic disorders (MASH, diabetes, cardiac hypertrophy). BAAT, CS/MDH1/H6PD, and SRC/MAPK14/EMD/ITGB1 were identified as mechanistic biomarkers for these conditions.

Then in vivo results indicated that downregulation of ANXA1 in B-ALL cells could significantly reduce leukemic cell burden and increase dexamethasone sensitivity. Therefore, ANXA1 was identified as an oncogene in the development and progression of B-ALL and might be a promising biomarker for treating B-ALL.

Specifically, AdipoRon preferentially suppressed ACC1 expression and subsequently downregulated CPT1A, indicating disruption of fatty acid metabolism. These findings establish that AdipoRon suppresses MM progression through AMPK-driven metabolic reprogramming and apoptosis induction, positioning adiponectin receptor agonism as a promising therapeutic strategy for multiple myeloma.

This approach effectively suppressed CRPC xenograft tumor growth, even in models resistant to next-generation ARSIs. This study reveals an AR-regulated circRNA involved in PCa progression and suggests a potential therapeutic strategy for treatment-resistant PCa.

Single-cell analysis indicated specific expression of AKR1C3 in HCC cells, while molecular docking analysis showed that, among the five potential targets, AKR1C3 demonstrated the most stable binding affinity to rutin. Our findings suggest that rutin may modulate ferroptosis in HCC, with rutin associated ferroptosis genes implicated in disease biology; moreover, the proposed risk scoring model shows promising prognostic utility in HCC.

Our findings reveal tissue-specific expression patterns of KIR genes that are differentially affected by chronic lentivirus infection, emphasizing the importance of compartmentalized KIR regulation in viral pathogenesis. This proof-of-concept study presents a reliable and scalable framework for the detailed characterization of the KIR gene repertoire in non-human primate models, providing a valuable alternative to traditional qPCR for profiling gene expression in complex tissues.