ArticleActa biochimica et biophysica Sinica2025
The ACSS2-PPARD-BCAT1 axis synchronously regulates branched-chain amino acid metabolism and development in pancreatic cancer.
Article in Acta biochimica et biophysica Sinica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Silencing of BCAT1 induces ferroptosis and inhibits brain metastasis of non-small cell lung cancer via activating the cGAS-STING pathway.Journal of thoracic disease · 2026Article
- BCAT1 inhibits glutamine-dependent Akt/mTOR signaling and nucleotide synthesis by initiating BTRC-mediated degradation of SLC3A2 in pancreatic adenocarcinoma.Cancer & metabolism · 2026Article
- In-silico study of machine learning discovers de novo lipogenesis for predicting prognosis and immunotherapy responses in kidney renal clear cell carcinoma.Biology direct · 2026Article
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11 authors.
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Abstract
The characteristics of the tumor microenvironment (TME) of pancreatic cancer include an abundant stroma, hypoxia, insufficient blood supply and high degree of immunosuppression. Therefore, overcoming the TME conditions to reach a hypermetabolic state is a concern for the treatment of pancreatic cancer. Previous studies have demonstrated that tumor cells adapt to the TME by activating or increasing the expression level of ACSS2 under metabolic stress. Our study focuses mainly on the relationship between ACSS2 and amino acid metabolism. We find that ACSS2 is generally highly expressed and promotes the proliferation and invasiveness of pancreatic cancer. Knockout of
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