Bcat1
- Known as:
- Bcat1
- Catalog number:
- 065935A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Bcat1
Related genes to: Bcat1
- Gene:
- BCAT1 NIH gene
- Name:
- branched chain amino acid transaminase 1
- Previous symbol:
- BCT1
- Synonyms:
- -
- Chromosome:
- 12p12.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-03-07
Related products to: Bcat1
Related articles to: Bcat1
- Thyroid cancer (TC) dedifferentiation contributes to tumor progression, treatment resistance, and poor survival, yet the underlying molecular mechanisms remain elusive. Genetic alterations, copy number variations, and epigenetic modifications may contribute to this process. Here, we conducted an integrated analysis to screen for critical molecules involved in TC dedifferentiation, identifying nucleolar and spindle-associated protein 1 (NUSAP1) as a candidate. NUSAP1 is overexpressed in TC and associated with poor prognosis. Upregulation of NUSAP1 enhances TC cell proliferation, migration, and dedifferentiation, evidenced by the suppression of thyroid differentiation genes and the induction of epithelial-mesenchymal transition. Mechanistically, branched-chain amino acid (BCAA) catabolism is a potential mechanism of dedifferentiation in TC mediated by NUSAP1 through RNA sequencing enrichment analysis. Specifically, NUSAP1 forms a transcriptional complex with bromodomain containing 4 (BRD4), which activates branched-chain amino acid transaminase 1 (BCAT1) transcription and leads to accelerated BCAA catabolism and reduced α-ketoglutarate (α-KG) levels. This metabolic shift increases histone H3 lysine 27 trimethylation (H3K27me3) levels by impairing histone demethylation, thereby suppressing the expression of thyroid differentiation genes. Pharmacologic inhibition of NUSAP1 with entinostat suppresses downstream target levels, suggesting a novel treatment modality. In summary, NUSAP1 promotes dedifferentiation through the BCAT1/α-KG/H3K27me3 axis by forming a transcriptional complex with BRD4, which indicates that NUSAP1 is a potential therapeutic target in TC. - Source: PubMed
Publication date: 2026/06/11
Wang YueWang GuorongZhao XuziWang GuangzhiYang FengyuanZhao YanWang ZhechengWang YiZhang NingYao JihongTian Xiaofeng - Colorectal cancer (CRC) metastasis is a major cause of cancer‑related death, highlighting the need for therapies that target immune‑metabolic pathways. Here, we show that quercetin inhibits CRC progression via dual actions: directly suppressing tumor cell growth and migration, while systemically reinvigorating CD8 T cell mediated immunity. In vitro, quercetin potently inhibited CRC cell proliferation, migration, and survival. In an experimental lung metastasis mouse model, quercetin enhanced the effector function of CD8 T cells, as evidenced by increased production of Granzyme B, Perforin, and IFN-γ in metastases, blood, and tumor-draining lymph nodes. Metabolomic profiling uncovered a pronounced remodeling of branched-chain amino acid (BCAA) metabolism following quercetin intervention. Screening via the HERB database identified BCAA transaminase 1 (BCAT1) as a candidate target, confirmed by molecular docking and surface plasmon resonance (SPR). Importantly, the combination of oral leucine and quercetin produced a synergistic effect, significantly boosting CD8 T cell cytotoxicity and dramatically reducing the lung metastatic burden. Taken together, these data identify BCAT1 as a direct target of quercetin and elucidate a resultant immunometabolic circuit that bolsters CD8 T cell function, providing a rationale for targeting this pathway in advanced CRC. - Source: PubMed
Publication date: 2026/06/05
Wang ChuyiXu YunxingDing PengchengDing YunhaiZheng LiangfengLi TianyiCheng ShouliangZhang ChenJi FeiyueLiu XiaojiangChen KaiGu GuiyuanLu Xiaomin - Bisphenols (including BPA, BPF, BPS, BPAF and TBBPA) are ubiquitous environmental endocrine disruptors linked to increased risk of multiple malignancies, yet their carcinogenic mechanisms remain poorly understood. To address this gap, the present study aimed to elucidate how bisphenols drive osteosarcoma initiation and progression, identify core mediating targets, and explore their pan-cancer relevance. We integrated network toxicology with osteosarcoma transcriptome datasets to screen hub genes, validated candidates via independent cohorts and machine learning, and pinpointed the core target through combined SHapley Additive Explanations (SHAP) and Weighted Gene Co-expression Network Analysis (WGCNA). Using data from The Cancer Genome Atlas (TCGA), we analyzed the target's association with osteosarcoma patient survival, while reverse transcription quantitative polymerase chain reaction (RT-qPCR), RNA sequencing (RNA-seq), and Western blotting confirmed its differential expression in osteosarcoma cell lines versus normal osteoblasts. Additionally, we performed simulated BCAT1 gene knockout using scTenifoldKnk to investigate its regulatory effects on downstream gene networks. Molecular docking and all-atom molecular dynamics simulations assessed bisphenol-target binding affinity, complemented by comprehensive pan-cancer analyses of public omics databases. Bioinformatic analyses identified branched-chain amino acid transaminase 1 (BCAT1) as the key regulatory gene, with experimental validation confirming its marked upregulation in osteosarcoma cells. All five bisphenols exhibited high binding affinity for BCAT1 in structural simulations, and pan-cancer analysis revealed BCAT1 overexpression in multiple solid tumors, correlating with unfavorable clinical outcomes. Collectively, these findings suggest that bisphenols may act as potential regulators of BCAT1, with implications for tumor progression, though further experimental validation is required to confirm the actual enzymatic activity modulation and carcinogenic effects. - Source: PubMed
Publication date: 2026/06/09
Jiahao SunCong WangXin LiXu CuiWenpeng XieYongkui Zhang - Acute-on-chronic liver failure (ACLF) is characterized by profound metabolic dysfunction and high mortality. Identifying amino acid metabolism-related biomarkers is crucial for early diagnosis and therapeutic intervention. Amino acid metabolism-related genes (AAMGs) and ACLF transcriptomic data were integrated to identify core genes via weighted gene co-expression network analysis (WGCNA) and differential expression analysis. Three machine learning (ML) algorithms-Random Forest, SVM-RFE, and Boruta-were applied to screen hub genes. Specific cellular profiles and immune landscapes were characterized using single-cell RNA sequencing (scRNA-seq) and ssGSEA. The pathological role of BCAT1 was investigated in APAP-induced ACLF models. A total of 26 genes were identified at the intersection of module genes, DEGs, and AAMGs. ML confirmed a three-gene signature (BCAT1, RPS6, OAT) with high diagnostic accuracy. ScRNA-seq analysis further verified that BCAT1 is predominantly expressed in hepatocytes, indicating its cell-type specific role in liver injury progression. In vitro and in vivo experiments demonstrated that BCAT1 exacerbates hepatocyte injury by activating the GSDMD/Caspase-1-mediated pyroptosis pathway. Our study reveals that BCAT1 is a pivotal driver of hepatocyte pyroptosis in ACLF. Targeting the BCAT1-mediated metabolic-inflammatory axis offers a promising therapeutic strategy for managing ACLF. - Source: PubMed
Li MengyueLu BinChen XingzhiKang ManqiuWang GangWang LifengYe HuowangPu FulinWang MeiqianWen WeihengChen Yiru - Colorectal cancer (CRC) treatment failure results in high mortality. The current CRC treatment response monitoring blood biomarker carcinoembryonic antigen (CEA) lacks specificity. Methylated BCAT1/IKZF1 circulating tumour DNA (ctDNA) indicates CRC, but its utility during therapy is uncertain. This study examined whether during-treatment measurement of BCAT1/IKZF1 ctDNA reflects CRC treatment efficacy. - Source: PubMed
Publication date: 2026/06/02
Rafeeu RafhaSymonds Erin LMichael Michael ZCornthwaite KathrynPedersen Susanne KSmith Renee JYoung Graeme PWinter Jean M