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Pancreatic cancer: branched-chain amino acids as putative key metabolic regulators?
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SYSNO ASEP 0553167 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Pancreatic cancer: branched-chain amino acids as putative key metabolic regulators? Author(s) Rossmeislová, L. (CZ)
Gojda, J. (CZ)
Smolková, Katarína (FGU-C) RID, ORCID, SAISource Title Cancer and Metastasis Reviews. - : Springer - ISSN 0167-7659
Roč. 40, č. 4 (2021), s. 1115-1139Number of pages 25 s. Language eng - English Country NL - Netherlands Keywords PDAC ; cancer cachexia ; insulin resistance ; adipose tissue ; BCAA metabolism OECD category Endocrinology and metabolism (including diabetes, hormones) R&D Projects NV19-01-00101 GA MZd - Ministry of Health (MZ) Method of publishing Limited access Institutional support FGU-C - RVO:67985823 UT WOS 000735340900001 EID SCOPUS 85121865652 DOI 10.1007/s10555-021-10016-0 Annotation Branched-chain amino acids (BCAA) are essential amino acids utilized in anabolic and catabolic metabolism. While extensively studied in obesity and diabetes, recent evidence suggests an important role for BCAA metabolism in cancer. Elevated plasma levels of BCAA are associated with an increased risk of developing pancreatic cancer, namely pancreatic ductal adenocarcinoma (PDAC), a tumor with one of the highest 1-year mortality rates. The dreadful prognosis for PDAC patients could be attributable also to the early and frequent development of cancer cachexia, a fatal host metabolic reprogramming leading to muscle and adipose wasting. We propose that BCAA dysmetabolism is a unifying component of several pathological conditions, i.e., obesity, insulin resistance, and PDAC. These conditions are mutually dependent since PDAC ranks among cancers tightly associated with obesity and insulin resistance. It is also well-established that PDAC itself can trigger insulin resistance and new-onset diabetes. However, the exact link between BCAA metabolism, development of PDAC, and tissue wasting is still unclear. Although tissue-specific intracellular and systemic metabolism of BCAA is being intensively studied, unresolved questions related to PDAC and cancer cachexia remain, namely, whether elevated circulating BCAA contribute to PDAC etiology, what is the biological background of BCAA elevation, and what is the role of adipose tissue relative to BCAA metabolism during cancer cachexia. To cover those issues, we provide our view on BCAA metabolism at the intracellular, tissue, and whole-body level, with special emphasis on different metabolic links to BCAA intermediates and the role of insulin in substrate handling. Workplace Institute of Physiology Contact Lucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400 Year of Publishing 2022 Electronic address https://doi.org/10.1007/s10555-021-10016-0
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