Format

Send to

Choose Destination
Life Sci. 2015 Aug 1;134:49-55. doi: 10.1016/j.lfs.2015.05.016. Epub 2015 May 31.

Curcumin inhibits Ec109 cell growth via an AMPK-mediated metabolic switch.

Author information

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.

KEYWORDS:

AMPK; Curcumin; Ec109 cell; Glycolytic enzymes; Metabolic reprogramming

PMID:
26037398
DOI:
10.1016/j.lfs.2015.05.016
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center