Feng-Juan Zhang1, Hong-Sheng Zhang2, Yang Liu1, Ying-Hui Huang3. 1. College of Life Science & Bioengineering, Beijing University of Technology, Pingleyuan 100(#), District of Chaoyang, Beijing 100124, China. 2. College of Life Science & Bioengineering, Beijing University of Technology, Pingleyuan 100(#), District of Chaoyang, Beijing 100124, China. Electronic address: zhanghs@bjut.edu.cn. 3. College of Life Science & Bioengineering, Beijing University of Technology, Pingleyuan 100(#), District of Chaoyang, Beijing 100124, China. Electronic address: yhuang@bjut.edu.cn.
Abstract
AIMS: Glycolytic enzymes are always greatly increased in cancer cells. Whether metabolic reprogramming is involved in curcumin-mediated inhibition of cancer cell growth is unknown. MAIN METHODS: In this study, cell viability was assayed with MTS analysis; cell cycle was measured with flow cytometry analysis. RT-PCR and western blotting were used to analyse the mRNA and protein expression, respectively. KEY FINDINGS: Here we demonstrated that curcumin inhibited cancer cell growth, especially for Ec109 cells. Curcumin induced cell cycle arrest at G2/M phase. Curcumin caused a significant down-regulation of glycolytic enzymes expressions in a dose-dependent manner. Our results further indicated that the AMPK was required for curcumin-mediated down-regulation of glycolytic enzymes. AMPK-mediated down-regulation of glycolytic enzymes blocked Ec109 cell growth. SIGNIFICANCE: Taken together, our results revealed that the AMPK-mediated metabolic switch plays an important role in esophageal cancer cell growth.
AIMS: Glycolytic enzymes are always greatly increased in cancer cells. Whether metabolic reprogramming is involved in curcumin-mediated inhibition of cancer cell growth is unknown. MAIN METHODS: In this study, cell viability was assayed with MTS analysis; cell cycle was measured with flow cytometry analysis. RT-PCR and western blotting were used to analyse the mRNA and protein expression, respectively. KEY FINDINGS: Here we demonstrated that curcumin inhibited cancer cell growth, especially for Ec109 cells. Curcumin induced cell cycle arrest at G2/M phase. Curcumin caused a significant down-regulation of glycolytic enzymes expressions in a dose-dependent manner. Our results further indicated that the AMPK was required for curcumin-mediated down-regulation of glycolytic enzymes. AMPK-mediated down-regulation of glycolytic enzymes blocked Ec109 cell growth. SIGNIFICANCE: Taken together, our results revealed that the AMPK-mediated metabolic switch plays an important role in esophageal cancer cell growth.