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Open AccessArticle

Effect of 6-Shogaol on the Glucose Uptake and Survival of HT1080 Fibrosarcoma Cells

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Department of Nutrition and Biochemistry, School of Sciences, Pontificia Universidad Javeriana, Bogotá 110231, Colombia
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Department of Chemistry, School of Sciences, Pontificia Universidad Javeriana, Bogotá 110231, Colombia
*
Authors to whom correspondence should be addressed.
Pharmaceuticals 2019, 12(3), 131; https://doi.org/10.3390/ph12030131
Received: 4 July 2019 / Revised: 10 August 2019 / Accepted: 3 September 2019 / Published: 9 September 2019
Ginger is a plant that is native to southern China. In the last decade and research on the components of ginger has significantly increased; of these components, 6-shogaol exhibits the greatest potential antitumor capacity. However, the molecular mechanism through which 6-shogaol exerts its effects has not yet been elucidated. In this study, the effect of 6-shogaol on tumor cells that were derived from human fibrosarcoma (HT1080) was evaluated. Cell viability was determined by a (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) MTT assay testing different concentrations of 6-shogaol (2.5–150 μM). Subsequently, the effect of 6-shogaol on reactive oxygen species (ROS) production, glucose uptake, and protein expression of the signaling pathway phosphatase and tensin homolog/ protein kinase B /mammalian target of rapamycin (PTEN/Akt/mTOR) was measured. 6-Shogaol reduced the viability of the tumor cells and caused an increase in ROS production, which was attenuated with the addition of N-acetylcysteine, and the recovery of cell viability was observed. The increase in ROS production in response to 6-shogaol was associated with cell death. Similarly, glucose uptake decreased with incremental concentrations of 6-shogaol, and an increase in the expression of mTOR-p and Akt-p proteins was observed; PTEN was active in all the treatments with 6-shogaol. Thus, the results suggest that cells activate uncontrolled signaling pathways, such as phosphoinositide 3-kinase (PI3K)/Akt/mTOR, among other alternative mechanisms of metabolic modulation and of survival in order to counteract the pro-oxidant effect of 6-shogaol and the decrease in glucose uptake. Interestingly, a differential response was observed when non-cancerous cells were treated with 6-shogaol. View Full-Text
Keywords: 6-shogaol; HT1080; ROS; survival; glucose 6-shogaol; HT1080; ROS; survival; glucose
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MDPI and ACS Style

Romero-Arias, A.C.; Sequeda-Castañeda, L.G.; Aristizábal-Pachón, A.F.; Morales, L. Effect of 6-Shogaol on the Glucose Uptake and Survival of HT1080 Fibrosarcoma Cells. Pharmaceuticals 2019, 12, 131.

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