ACACB (Acetyl-CoA Carboxylase Beta)

143B cell experiments and qRT-PCR validated findings. MFH-derived compounds, especially ellagic acid dihydrate, have multi-target anti-OS potential, laying a foundation for novel OS therapeutics.

This study constructed and validated a metabolism-driven prognostic model. The model enables prognostic stratification of LGG patients and links high-risk scores to metabolic dysregulation and an immunosuppressive microenvironment characterized by M2 macrophage enrichment, based on multi-omics data. Mechanistic exploration indicates this association is particularly pronounced in myeloid cells, predominantly within metabolism-related M2 macrophage subpopulations. Furthermore, computational analysis suggests differences in drug sensitivity between risk groups and identifies potential therapeutic compounds, providing clues for future exploration of therapeutic strategies targeting metabolic-immune interactions.

These 4 genes were selected as hub genes as they are closely related to gluconeogenesis, the tricarboxylic acid cycle, lipid metabolism, amino acid metabolism and other mitochondrial metabolic pathways in PCa. In conclusion, 4 novel mitochondrial-related gene signatures that influence mitochondrial metabolism within the immune microenvironment were identified in PCa.

We have previously reported a structure-activity study of substituted oxindoles based on the multi-kinase inhibitor sunitinib to determine the structural requirements for AMPK inhibition and found that a 5-(2-cyanoethyl)-substituted oxindole displayed selectivity for AMPK over VEGFR-2...Here, we report a further series of 3,5-substituted oxindoles that demonstrate that 5-cyano-oxindoles can inhibit both GSK3β and AMPK, but the 5-(2-cyanoethyl)-substitution and the orientation of the 3-substituent of the oxindole are critical determinants for AMPK inhibition and selectivity. These findings could have critical importance in evaluating metabolic targeting in cancer as GSK3β promotes anabolic pathways and suppresses AMPK activity.

Our results suggest that our tree shrew model can faithfully replicate key characteristics of oxaliplatin-induced fatty liver disease, and that such disease involves oxidative stress and lipid dysmetabolism in the liver as well as dysbiosis of microbiota in the gut.

Cellular assays confirmed that dabrafenib effectively inhibited CRC cell migration and proliferation, providing a promising therapeutic avenue. Our findings suggested that the four mitochondrial-related genes identified in this study provide accurate survival predictions for CRC patients.

In this study, ADH1A, ACACB, CD36, CERS4, PDE3B, ALOX5, and CRAT were identified as biomarkers for PC, with their expression levels validated in clinical samples. These findings offered a potential theoretical foundation for developing targeted treatments for PC.

The stability of these complexes was validated by a 100 ns simulation run, and their binding free energy calculation was determined by MM-PBSA method. Interestingly, SE modulated the mRNA expression of genes involved in LMR in BC cell lines, MCF-7 and MDA-MB-231, thereby suggesting its potential as an inhibitor of LMR.

The prognostic signature derived from these genes represents a valuable tool for predicting clinical outcomes and guiding personalized treatment strategies. Among these, SCD stands out as a promising therapeutic target for PTC, warranting further research to validate these findings and uncover its underlying molecular mechanisms.

A reliable predictive signature based on genes related to fatty acid metabolism in endometrial cancer was conducted, wherein TEKT1 was mainly implicated as the primary gene of interest. TEKT1 showed affinity to AMPK-γ and probably promoted FA synthesis in endometrial cancer.

Leveraging bioinformatics and ML, this study identified four pivotal genes with significant diagnostic capabilities for DLBCL and HNSCC. The survival analysis corroborates their diagnostic accuracy, supporting the development of a diagnostic nomogram to assist in clinical decision-making.

ACC inhibition exacerbated DEN-induced liver tumorigenesis only when both ACC isotypes were completely inhibited. The pro-tumour phenotype of ACC inhibition was strongly reproducible irrespective of chow or high fat feeding, and irrespective of ACC inhibition prior to or after DEN treatment. Retaining partial ACC activity at either isotype prevented tumour exacerbation in mice at risk for developing liver tumours.