Bcat1 siRNA_Lentivectors
- Known as:
- Bcat1 siRNA_Lentivectors
- Catalog number:
- i065399b
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Bcat1 siRNA_Lentivectors
Related genes to: Bcat1 siRNA_Lentivectors
- 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 siRNA_Lentivectors
Related articles to: Bcat1 siRNA_Lentivectors
- Branched-chain amino acid (BCAA) transaminase 1 (BCAT1), the rate-limiting enzyme in BCAA metabolism, serves a pivotal role in tumor progression. Astragaloside IV (AS-IV) exhibits potential antitumor properties; however, whether AS-IV suppresses breast cancer migration by modulating BCAA metabolism via BCAT1 remains to be elucidated. The present study aimed to investigate whether AS-IV inhibits the invasion and migration of MDA-MB-231 triple-negative breast cancer (TNBC) cells by targeting BCAT1-mediated BCAA metabolic reprogramming. The present study used network pharmacology to predict AS-IV targets against breast cancer invasion, followed by BCAT1 knockdown and overexpression in MDA-MB-231 cells. Using molecular docking, cellular thermal shift assay, wound healing, Transwell, western blotting, quantitative PCR and liquid chromatography-mass spectrometry metabolomics, the present study systematically evaluated: i) AS-IV-BCAT1 direct binding and protein stability; ii) BCAA metabolic flux regulation via the branched-chain α-ketoacid dehydrogenase kinase (BCKDK)/branched-chain α-ketoacid dehydrogenase (BCKDH) axis; and iii) functional impacts on breast cancer cell migration and invasion. Network pharmacology predicted BCAT1 as a key potential target of AS-IV, with significant enrichment of the BCAA metabolic pathway. The results of the present study suggested that AS-IV binds to and stabilizes BCAT1 , an effect that is associated with reduced migration and invasion of MDA-MB-231 cells. It also promotes BCAA degradation via the BCKDK/BCKDH axis, lowering intracellular BCAA levels and suppressing malignancy. Notably, AS-IV maintained dose-dependent inhibition even with BCAT1 knockdown or overexpression, albeit with reduced efficacy. In conclusion, the present study suggested that AS-IV suppresses MDA-MB-231 cell invasion and migration by targeting BCAT1-mediated BCAA metabolism. These findings support further evaluation of AS-IV in TNBC and highlight BCAA metabolism as a potential intervention point in future research. - Source: PubMed
Publication date: 2026/08/03
Liu Yi-TingZhang LuSun Xiao-Dong - Primary cutaneous T-lymphomas (CTCL), particularly in their early stages, frequently present with clinical and histopathologic features that overlap with atopic dermatitis (AD) and psoriasis, contributing to diagnostic delay and ineffective, or even deleterious, treatment approaches. Thus, minimally invasive molecular tests capable of distinguishing CTCL from benign inflammatory dermatoses are urgently needed. - Source: PubMed
Publication date: 2026/08/07
Fleischli AbigailBar JonathanManson MeredithNg Brandon DMeledathu ShannonBurnett AmeliaChefitz GabriellaEstrada Yeriel DGour DigpalCices AhuvaCorrea da Rosa JoelBrunner Patrick MGuttman-Yassky Emma - Global sperm concentration has declined by over 50% in the past five decades, with environmental pollutants identified as a critical driving factor. This review focuses on testicular-level evidence regarding the effects of microplastics, bisphenol compounds, and air pollution on male reproductive health, with an emphasis on spermatogenic and testicular somatic cell mechanisms. Microplastics have been detected in human testicular tissue, with a causal pathway established linking gut microbiota dysbiosis, immune activation, and blood-testis barrier disruption. Bisphenol A substitutes show comparable or greater reproductive toxicity than BPA, with BCAT1-mediated ferroptosis identified as a novel testicular injury mechanism. For air pollution, spermatogenesis stage I (70-90 days prior to semen collection) has been pinpointed as the critical PM2.5 exposure vulnerability window, with metal constituents of traffic-derived PM2.5 as the primary toxicity drivers. Future research should prioritize prospective cohort studies and clinical intervention trials targeting these emerging mechanistic pathways. - Source: PubMed
Publication date: 2026/08/04
Guo AndongLu YiGuo YeLi Hongjun - Myofibroblasts are the cells responsible for collagen production, leading to tissue fibrosis. Because 20.5% of the total amino acids in collagen are proline, myofibroblasts must acquire a well-developed proline-producing mechanism during their differentiation. However, the detailed mechanism for myofibroblasts to acquire and keep the developed proline biosynthesis machinery remains obscure. Here, we show branched-chain amino acid transaminase 1 (Bcat1) is up-regulated in a substantial subset of Postn-expressing proto-myofibroblast-like fibroblasts, transitional cells en route to fully differentiated myofibroblasts, as well as in myofibroblasts in the fibrotic heart and liver of mice and humans and promotes the proline production. The branched-chain amino acid (BCAA) production by BCAT1 promotes SMAD3 phosphorylation via HDAC5 phosphorylation at Ser488, thereby enhancing SMAD3-dependent transcription of proline biosynthesis-related genes, Aldh18a1, Pycr1, and Eprs, in proto-myofibroblast-like fibroblasts and myofibroblasts. In BCAT1-deficient mice, expression of proline biosynthesis-related genes is significantly attenuated in their hearts after myocardial infarction, resulting in decreased cardiac fibrosis. Moreover, BCAT1 inhibitor treatment of mice with myocardial infarction reduces cardiac fibrosis. Our results identified a BCAT1-mediated pathway that promotes collagen production via proline biosynthesis regulation in proto-myofibroblast-like fibroblasts and myofibroblasts, which may provide a therapeutic target for cardiac fibrosis. - Source: PubMed
Publication date: 2026/07/16
Takizawa NoburoHironaka TakanoriWatanabe HayatoSuetsugu HarunaYoshioka KeisukeHorii YumaNagata YuriMatoba HiroakiKosako HidetakaHamase KenjiHirai GoNakaya Michio - Based on emerging evidence implicating branched-chain aminotransferase 1 (BCAT1) in tumorigenesis from animal and cellular studies, this study aimed to systematically evaluate its oncogenic role through a pan-cancer analysis to address the lack of comprehensive pan-cancer investigations in the literature. Using datasets from The Cancer Genome Atlas and the Genotype-Tissue Expression project, we analyzed BCAT1 expression, prognosis, genetic alterations, immune infiltration, and functional enrichment across 33 cancer types. The primary endpoints were overall survival (OS) and disease-free survival (DFS). Statistical significance was primarily defined as P < .05. For analyses involving multiple correlations across cancer and immune cell types, the false discovery rate < 0.05 was applied. BCAT1 was significantly upregulated in most malignancies, and high expression was associated with worse OS and DFS in multiple cancer types. BCAT1 expression correlated with reduced CD8+ T cell infiltration and increased cancer-associated fibroblast accumulation across several tumors. Enrichment analyses suggested BCAT1 involvement in RNA metabolism and intracellular protein processing. BCAT1 was significantly upregulated in most malignancies, and high expression was associated with worse OS and DFS in multiple cancer types, including adrenocortical carcinoma (hazard ratio = 6.3) and lower-grade glioma (hazard ratio = 2.6) (all log-rank P < .05), highlighting its potential as a pan-cancer biomarker and therapeutic target. The present findings are associative and require further experimental and external validation. - Source: PubMed
Wang BinbinWei YizeDong MingjieGao CongrongYue HuiSun Ming