Complementary ACSL isoforms contribute to a non-Warburg advantageous energetic status characterizing invasive colon cancer cells
Entity
UAM. Departamento de Química Física AplicadaPublisher
Nature Publishing GroupDate
2017-09-11Citation
10.1038/s41598-017-11612-3
Scientific Reports 7 (2017): 11143
ISSN
2045-2322DOI
10.1038/s41598-017-11612-3Funded by
This work was supported by MINECO (Plan Nacional I + D + i AGL2013-48943-C2 and AGL2016-76736-C3), CAM (P2013/ABI-2728, ALIBIRD-CM) and EU Structural FundsProject
Gobierno de España. AGL2013-48943-C2; Gobierno de España. AGL2016-76736-C3; Comunidad de Madrid. P2013/ABI2728/ALIBIRDEditor's Version
https://doi.org/10.1038/s41598-017-11612-3Subjects
Metabolic; Isoforms; ACSL1/ACSL4/SCD; Enzymes; Ciencia y Tecnología de AlimentosRights
© The Author(s) 2017Abstract
Metabolic reprogramming is one of cancer hallmarks. Here, we focus on functional differences
and individual contribution of acyl coA synthetases (ACSL) isoforms to the previously described ACSL/stearoyl-CoA desaturase (ACSL1/ACSL4/SCD) metabolic network causing invasion and poor prognosis in colorectal cancer (CRC). ACSL4 fuels proliferation and migration accompanied by a more glycolytic phenotype. Conversely, ACSL1 stimulates invasion displaying a lower basal respiratory rate. Acylcarnitines elevation, polyunsaturated fatty acids (PUFA) lower levels, and monounsaturated fatty acids (MUFA) upregulation characterize the individual overexpression of ACSL1, ACSL4 and SCD, respectively. However, the three enzymes simultaneous overexpression results in upregulated phospholipids and urea cycle derived metabolites. Thus, the metabolic effects caused by the network are far from being caused by the individual contributions of each enzyme. Furthermore, ACSL/SCD network produces more energetically efficient cells with lower basal respiration levels and upregulated creatine pathway. These features characterize other invasive CRC cells, thus, ACSL/SCD network exemplifies specific metabolic adaptations for invasive cancer cells
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Google Scholar:Sánchez-Martínez, Ruth
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Cruz-Gil, Silvia
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García-Álvarez, María Soledad
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Reglero Rada, Guillermo J.
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Ramírez de Molina, Ana
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