Overexpression and proliferation dependence of acyl‑CoA thioesterase 11 and 13 in lung adenocarcinoma

  • Authors:
    • Jen‑Yu Hung
    • Shyh‑Ren Chiang
    • Kuan‑Ting Liu
    • Ming‑Ju Tsai
    • Ming‑Shyan Huang
    • Jiunn‑Min Shieh
    • Meng‑Chi Yen
    • Ya‑Ling Hsu
  • View Affiliations

  • Published online on: July 18, 2017     https://doi.org/10.3892/ol.2017.6594
  • Pages: 3647-3656
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Abstract

The metabolites of fatty acyl‑Coenzyme A (CoA) and metabolic enzymes contribute to lipid biosynthesis, signal transduction, and gene transcription. Previous studies have indicated that elevated concentrations of specific free fatty acids in the plasma and overexpression of specific fatty acyl‑CoA metabolic enzymes are observed in patients with lung adenocarcinoma. However, there are >30 enzymes in this metabolic network and have been fully investigated. In the present study, the expression levels of enzymes in the acyl‑CoA synthetase (ACS) and acyl‑CoA thioesterase (ACOT) families were analyzed from six microarray expression datasets that were collected from Gene Expression Omnibus. Compared with adjacent non‑tumor lung tissue, lung adenocarcinoma tissue exhibited significantly higher ACOT11 and ACOT13 expression. Kaplan‑Meier plotter database analysis demonstrated that high levels of ACOT11 and ACOT13 were associated with a worse overall survival rate. The proliferation of the lung adenocarcinoma cell lines CL1‑0 and CL1‑5 was inhibited when ACOT11 and ACOT13 were downregulated by short hairpin RNA. Although ACOT11 and ACOT13 knockdown did not significantly affect the total amount of intracellular and medium‑free fatty acids, ACOT11 and ACOT13 knockdown-mediated growth inhibition was rescued by the addition of fatty acids. In conclusion, ACOT11 and ACOT13 were upregulated in clinical specimens of lung adenocarcinoma, which may contribute to increased cell proliferation through the increased availability of fatty acids. The metabolites of the two enzymes may be critical for development of lung adenocarcinoma.
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September-2017
Volume 14 Issue 3

Print ISSN: 1792-1074
Online ISSN:1792-1082

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Spandidos Publications style
Hung JY, Chiang SR, Liu KT, Tsai MJ, Huang MS, Shieh JM, Yen MC and Hsu YL: Overexpression and proliferation dependence of acyl‑CoA thioesterase 11 and 13 in lung adenocarcinoma. Oncol Lett 14: 3647-3656, 2017.
APA
Hung, J., Chiang, S., Liu, K., Tsai, M., Huang, M., Shieh, J. ... Hsu, Y. (2017). Overexpression and proliferation dependence of acyl‑CoA thioesterase 11 and 13 in lung adenocarcinoma. Oncology Letters, 14, 3647-3656. https://doi.org/10.3892/ol.2017.6594
MLA
Hung, J., Chiang, S., Liu, K., Tsai, M., Huang, M., Shieh, J., Yen, M., Hsu, Y."Overexpression and proliferation dependence of acyl‑CoA thioesterase 11 and 13 in lung adenocarcinoma". Oncology Letters 14.3 (2017): 3647-3656.
Chicago
Hung, J., Chiang, S., Liu, K., Tsai, M., Huang, M., Shieh, J., Yen, M., Hsu, Y."Overexpression and proliferation dependence of acyl‑CoA thioesterase 11 and 13 in lung adenocarcinoma". Oncology Letters 14, no. 3 (2017): 3647-3656. https://doi.org/10.3892/ol.2017.6594