Shuso Takeda1,2, Hiroyuki Okazaki2, Taichi Kudo2, Kazuhiro Kakizoe2, Taichi Himeno2, Kenji Matsumoto3, Mitsuru Shindo3, Hironori Aramaki4,5. 1. Laboratory of Xenobiotic Metabolism and Environmental Toxicology, Faculty of Pharmaceutical Sciences, Hiroshima International University (HIU), Hiroshima, Japan. 2. Department of Molecular Biology, Daiichi University of Pharmacy, Fukuoka, Japan. 3. Institute for Materials Chemistry and Engineering, Kyushu University, Kasuga, Japan. 4. Department of Molecular Biology, Daiichi University of Pharmacy, Fukuoka, Japan haramaki@daiichi-cps.ac.jp. 5. Drug Innovation Research Center, Daiichi University of Pharmacy, Fukuoka, Japan.
Abstract
BACKGROUND/AIM: An in vitro cell model of long-term estrogen-deprived MCF-7 (LTED) cells has been utilized to analyze the re-growth mechanisms of breast cancers treated with blockers for estrogen receptor α (ERα) signaling. Bongkrekic acid (BKA) is a natural toxin isolated from coconut tempeh contaminated with the bacterium Burkholderia cocovenans. MATERIALS AND METHODS: LTED cells, MCF-7 cells and MDA-MB-231 cells were employed in the study. After treatment with BKA (chemically synthesized; purity: >98%), several biochemical analyses were carried out. RESULTS: LTED cells were categorized into an oxidative phenotype. When LTED cells were treated with BKA, lactate dehydrogenase A (LDH-A)/pyruvate dehydrogenase kinase 4 (PDK4) were down-regulated, thereby prompting the aggressive use of glucose via mitochondrial oxidative phosphorylation and induction of cell death responses. These effects of BKA were not observed in the other breast cancer cells analyzed. CONCLUSION: We suggest the potential of BKA as an experimental tool for the analysis of cancer biology in LTED cells. Copyright
BACKGROUND/AIM: An in vitro cell model of long-term estrogen-deprived MCF-7 (LTED) cells has been utilized to analyze the re-growth mechanisms of breast cancers treated with blockers for estrogen receptor α (ERα) signaling. Bongkrekic acid (BKA) is a natural toxin isolated from coconut tempeh contaminated with the bacterium Burkholderia cocovenans. MATERIALS AND METHODS: LTED cells, MCF-7 cells and MDA-MB-231 cells were employed in the study. After treatment with BKA (chemically synthesized; purity: >98%), several biochemical analyses were carried out. RESULTS: LTED cells were categorized into an oxidative phenotype. When LTED cells were treated with BKA, lactate dehydrogenase A (LDH-A)/pyruvate dehydrogenase kinase 4 (PDK4) were down-regulated, thereby prompting the aggressive use of glucose via mitochondrial oxidative phosphorylation and induction of cell death responses. These effects of BKA were not observed in the other breast cancer cells analyzed. CONCLUSION: We suggest the potential of BKA as an experimental tool for the analysis of cancer biology in LTED cells. Copyright
Authors: Maheedhara R Guda; Swapna Asuthkar; Collin M Labak; Andrew J Tsung; Ilya Alexandrov; Malcolm J Mackenzie; Durbaka Vr Prasad; Kiran K Velpula Journal: Am J Cancer Res Date: 2018-09-01 Impact factor: 6.166