ACADSB (Acyl-CoA Dehydrogenase Short/Branched Chain)

Additionally, LPAL2 decreased YBX1 stability by promoting its ubiquitination-mediated degradation, while YBX1 inhibited the transcription of certain BCAA catabolic enzymes through binding to their promoters. In summary, the LPAL2-YBX1 interaction regulates BCAA metabolism to influence GBC cell proliferation, which could be targeted for therapeutic interventions in GBC treatment.

Tier 3 proteins, supported by logistic regression and MR only, included CD5L, GNPDA, ACAN, C7, DMP1, HEPH, CEACAM6, COX6B1, CPXM2 and IL12RB2. Druggability evaluation suggests that existing drugs targeting ITGB2, GP1BA, ACADSB and COX6B1 could potentially be repurposed for the treatment of specific lung cancer subtypes.

Our mitochondrial-related gene signature, as a risk model, could be a reliable ccRCC prognostic biomarker and could predict the response to immunotherapy. The risk score was correlated with the tumor microenvironment and immune cell infiltration.

Drug analyses suggested cisplatin and sunitinib downregulated oncogenic targets. Silencing ABCB1 or AKR1C3, or overexpressing LDHB, suppressed KIRC cell proliferation and migration in vitro; LDHB overexpression combined with sorafenib significantly reduced tumor growth in vivo. We propose a robust immunometabolism-based diagnostic model and six experimentally supported biomarkers for KIRC, providing mechanistic insight into tumor-immune interactions and potential avenues for personalized therapy.

Our results suggest that the LMG signature may serve as a novel diagnostic tool for identifying patients with UC. Our machine-learning model may contribute to future research on the formulation of potential therapeutic strategies.

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.

In summary, this study proposes that tRF-23-Q99P9P9NDD may affect GC lipid metabolism and ferroptosis by targeting ACADSB, thereby promoting GC progression. It provides a theoretical basis for the diagnostic and prognostic monitoring value of GC and opens up new possibilities for treatment.

This study is expected to provide valuable references and potential drugs for future research and treatment of COVID-19 and ICC.

Finally, experimental validation verified that the migratory ability of MUM-2B cells was suppressed by the knockdown of the identified genes in vitro. We constructed a CRTG signature that is helpful in predicting prognosis and guiding treatment for patients with UVM.

In vitro luciferase assay demonstrated that the promoter activity of ACADSB was significantly increased in the rs12220683 variant C allele compared with that in the wild G allele (P = 3 × 10-5). These results suggest that ACADSB rs12220683G>C increases promoter activity and that increased ACADSB expression may result in better OS in patients with surgically resected NSCLC.