Targeting BCAT1 or disrupting its downstream mTOR/NF-κB signaling effectively inhibits PDAC pan-metastasis. These results uncover an unrecognized metabolic-immune crosstalk governing BCAT1+ metastasis-related tumor cells and pan-metastasis of PDAC.
Proof-of-principle experiments assessed CRC cell lines for BCAT1/IKZF1 methylation after irradiation and 5-fluorouracil treatment...Reduced BCAT1/IKZF1 methylation in rectal tumors and plasma ctDNA reflects reductions in tumor cellularity. These data support future investigations to use methylated BCAT1/IKZF1 ctDNA for monitoring response to neoadjuvant therapy in patients with rectal cancer.
Multivariate analysis further identified tumor size (OR = 1.974, 95% CI: 1.321-2.950, P = 0.005) and TNM stage (OR = 2.117, 95% CI: 1.452-3.087, P = 0.002) as independent predictors of multi-gene methylation positivity. Multi-gene methylation detection showed high diagnostic value for CRC and may serve as a valuable adjunct tool in CRC screening strategies.
The diagnostic sensitivities of the model for CRC of different stages were 85.71% for stage Ⅰ, 92.86% for stage Ⅱ, 78.95% for stage Ⅲ, and 87.50% for unstaged cases. A diagnostic model based on the methylation levels of the SEPTIN9, BCAT1, IKZF1, BCAN, and VAV3 genes in plasma demonstrates good diagnostic performance for CRC, particularly in early-stage cases.
DNA methylation and microRNA biomarkers hold strong promises for non-invasive CRC screening. Multi-marker panels demonstrate superior diagnostic accuracy and may provide a cost-effective, scalable approach for early CRC detection in resource-limited settings.
MAT2A, BCAT1 and GCLM were selected for small interfering RNA experiments and the results exhibited that apoptosis rates significantly promoted in HL60/R when MAT2A, BCAT1 or GCLM were interfered. An integrative analysis of proteomic and metabolomic data revealed significant disruptions in amino acid metabolism in HL60/R cells, including the metabolic pathways of alanine, aspartate and glutamate, cysteine and methionine, as well as glutathione metabolism.
Innovative therapeutic strategies targeting BCAA pathways-ranging from selective small-molecule inhibitors (e.g., LAT1 and BCAT1/2) to dietary modulation-have shown promising preclinical and early clinical efficacy, highlighting their potential to exploit metabolic vulnerabilities in cancer cells while bolstering immune responses. By integrating multi-omics data and precision targeting approaches, this review underscores the translational significance of BCAA metabolic reprogramming, positioning it as a novel frontier in cancer treatment.
DDX6 KO leads to rapid PB dissolution and release of PB-enriched mRNAs, such as BCAT1, into the cytosol, where these transcripts undergo degradation. By reducing BCAT1 levels, DDX6 KO reprograms amino acid metabolism and sensitizes AML cells to cytarabine chemotherapy.
Quantitative analysis of DNA methylation at CpG sites near the C3orf37 gene appears to be a promising approach to distinguish between index and indolent prostate cancer cells.
This study demonstrates the feasibility of applying behavioural science and SDM frameworks to analyse trial recruitment consultations. While a range of BCTs were identified, SDM efforts were generally low. Recruitment practices may benefit from more deliberate consideration of these techniques and greater emphasis on shared decision-making to support informed choices.
While gabapentin (Gp) can inhibit BCAA catabolism by targeting branched-chain amino acid aminotransferase 1 (BCAT1), its efficacy is limited by inefficient delivery and compensatory mitochondrial metabolism...Metabolomic analyses further confirmed synergistic BCAA metabolic inhibition and copper-induced mitochondrial dysfunction. This work presents a promising metabolic intervention strategy for pancreatic cancer through targeted nanomedicine.