期刊
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
卷 598, 期 -, 页码 50-56出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.abb.2016.03.031
关键词
Tanshinone IIA; PKM2; miR-122; Metabolic reprogramming
资金
- Importation and Development of High-Caliber Talents Project of Beijing Municipal Institutions [CITTCD201304054]
- National Natural Sciences Foundation of China [30800580]
- Beijing Natural Science Foundation [5112004, 5093025]
- Beijing Nova Program [2007B014]
Pyruvate kinase M2 (PKM2) plays a pivotal role in the growth, survival and metabolic reprogramming of cancer cells. Here, we presented for the first time that tanshinone IIA inhibited human esophagus cancer cell growth through miR-122-mediated PKM2 down-regulation pathway. Tanshinone IIA inhibited cell proliferation and induced cell cycle arrest in S phase in human Ec109 cells. As expected, tanshinone IIA down-regulated PKM2 mRNA and protein expression in Ec109 cells. Given these findings, we further investigated microRNAs regulation of PKM2 and confirmed miR-122 for targeting PKM2. Moreover, we found that tanshinone IIA-induced up-regulation of miR-122 expression inhibited PKM2 expression in Ec109 cells. Meanwhile, tanshinone IIA inhibited proliferation through miR122-medated PKM2 down regulation. It was demonstrated that the anticancer activity of tanshinone HA was targeted at metabolic regulation of miR-122/PKM2 in human esophagus cancer cells. Taken together, our results revealed tanshinone HA targeting at PKM2-mediated metabolic reprogramming play an important role in inhibition of esophageal cancer cell growth. (C) 2016 Elsevier Inc. All rights reserved.
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