Remodeling of energy metabolism by a ketone body and medium-chain fatty acid suppressed the proliferation of CT26 mouse colon cancer cells

Kadochi,Yui; Mori,Shiori; Fujiwara‑Tani,Rina; Luo,Yi; Nishiguchi,Yukiko; Kishi,Shingo; Fujii,Kiyomu; Ohmori,Hitoshi; Kuniyasu,Hiroki

doi:10.3892/ol.2017.6195

Remodeling of energy metabolism by a ketone body and medium-chain fatty acid suppressed the proliferation of CT26 mouse colon cancer cells

Authors:
- Yui Kadochi
- Shiori Mori
- Rina Fujiwara‑Tani
- Yi Luo
- Yukiko Nishiguchi
- Shingo Kishi
- Kiyomu Fujii
- Hitoshi Ohmori
- Hiroki Kuniyasu
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Affiliations: Department of Molecular Pathology, Nara Medical University, Kashihara, Nara 634‑8521, Japan
Published online on: May 17, 2017 https://doi.org/10.3892/ol.2017.6195
Pages: 673-680
Copyright: © Kadochi et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Normal and cancerous cells are suggested to have differential utilization of fatty acids and ketone bodies, which could be exploited in cancer therapy. The present study examined the effect of 3‑hydroxybutyric acid (3‑HBA), which is a ketone body generating acetyl‑CoA, and lauric acid (LAA, C12:0), which is a medium‑chain saturated fatty acid translocated to mitochondria in a carnitine‑independent manner to produce acetyl‑CoA, on the energy metabolism of mouse CT26 colon cancer cells. In CT26 cells expressing 3‑HBA and LAA transporters, 3‑HBA and LAA reduced cell proliferation, mitochondrial volume and lactate production, and increased oxidative stress, particularly in low‑glucose conditions. Concurrent treatment with 3‑HBA and LAA under glucose starvation had a synergistic effect on cell growth inhibition. In addition, LAA and LAA + 3‑HBA promoted an imbalance in the expression of enzymes in the electron transport chain. These findings suggested that treatment with 3‑HBA and/or LAA during glucose starvation may reprogram energy metabolism and decrease the proliferation of cancer cells.

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