ACADM (Acyl-CoA Dehydrogenase Medium Chain)

Nine of these genes showed significant prognostic relevance. The current work identifies key biomarkers that can enhance ccRCC diagnosis and guide future therapy.

GBHP01 may contribute to shifts in gut microbial composition by elevating probiotic species (L. reuteri and L. murinus) and reducing inflammatory taxa (Bilophila and Mucispirillum), suggesting its potential as a dietary intervention against HFD-induced metabolic disorders.

In vivo experiments showed that NFKB2 knockdown inhibited tumor growth and the expansion of CD8+PDCD1+ T cells, effects that were reversible with corticosterone treatment (all P < 0.05). Collectively, a glucocorticoid signaling-related gene signature was developed and rigorously validated as a predictive tool for prognosis and immunotherapeutic response in KIRC, offering valuable insights for guiding personalized treatment strategies.

EVs may act as tumor biomarkers in patients with PNS, even in intermediate-risk cases.

In addition, after analyzing the ROC curve, it was found that the combination of ACADM, KRT33B, and C14orf34 is the most practical combination of diagnostic markers. This combination achieved sensitivity, specificity, and Area Under the Curve (AUC) values of 0.92, 0.86, and 0.93, respectively.

Notably, inhibition of REGγ in the iWAT alleviates HFD-induced obesity, thereby identifying REGγ as a latent target for obesity treatment. Together, the findings provide new targets for intervening in obesity and might ultimately offer new options for treating obesity.

We successfully constructed a prognostic model for EWS related to fatty acid metabolism genes. PPT1 and ACOT7 may serve as promising predictors for EWS prognosis.

Down-regulation of ACADM inhibits migration and invasion ability of estrogen receptor-positive breast cancer cells by lowering lipotoxicity and impairing mitochondrial function through the ROS/PI3K/AKT pathway.

Drug sensitivity analysis suggested that AKT inhibitor III was more effective in the low-risk cohort, while Bortezomib might be more beneficial for high-risk patients...Methylation profiling of the core genes via the UALCAN platform revealed distinct epigenetic signatures in ccRCC, providing deeper insight into the disease's molecular mechanisms. This study contributes to a more comprehensive understanding of ccRCC and proposes valuable directions for personalized treatment strategies and enhanced patient management.

ACADM can regulate ferroptosis-related proteins (ACSL4, SLC7A11, and GPX4) to further influence the invasion and metastasis of CRC cells. This newly discovered mechanism provides potential therapeutic targets for CRC treatment and insights for controlling CRC progression and metastasis.

In conclusion, we explored the key sialylated glycoproteins, which may play a key role in tumor LNM and clinical outcomes. And constructed the LRSRGs-phenotype and signature with prognostic and therapeutic predictive value in CRC, hoping to provide reliable scientific basis for future treatments in CRC patients.

CLDN8 is downregulated in KIRC and is considered a potential tumor suppressor. CLDN8 deficiency may promote the initiation and progression of KIRC, potentially in conjunction with metabolic dysfunction.