ACACA (Acetyl-CoA Carboxylase Alpha)

Its mechanism of action involves the suppression of lipid synthesis and the prevention of hepatocyte apoptosis, achieved by modulating key anti-inflammatory and antioxidant signaling pathways. Flavonoids (such as apigenin and quercetin) are identified as the key active ingredients in DXR responsible for activating Keap1/Nrf2 and PI3K/AKT signaling pathways.

GL-V9 overcomes cisplatin resistance in ovarian cancer by targeting ACC1 and elevating ROS levels, highlighting its potential as a clinically translatable therapeutic strategy.

However, serum or prostate tumor level of acetyl-CoA or TFFA was not decreased by BMAX treatment. A longer duration treatment with BMAX in early-stage prostate cancer patients may be necessary to lower circulating or prostate tumor level of TFFA.

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.