| Literature DB >> 25818238 |
Kohei Taniguchi1, Nobuhiko Sugito2, Minami Kumazaki2, Haruka Shinohara2, Nami Yamada2, Yoshihito Nakagawa3, Yuko Ito4, Yoshinori Otsuki4, Bunji Uno2, Kazuhisa Uchiyama5, Yukihiro Akao6.
Abstract
Altered levels and functions of microRNAs (miRs) have been associated with carcinogenesis. In this study, we investigated the role of miR-124 in colorectal adenoma (CRA) and cancer (CRC). The expression levels of miR-124 were decreased in CRA (81.8%) and CRC (57.6%) in 55 clinical samples. The ectopic expression of miR-124 induced apoptosis and autophagy in colon cancer cells. Also, miR-124 targeted polypyrimidine tract-binding protein 1 (PTB1), which is a splicer of pyruvate kinase muscles 1 and 2 (PKM1 and PKM2) and induced the switching of PKM isoform expression from PKM2 to PKM1. Also, siR-PTB1 induced drastic apoptosis in colon cancer cells. Furthermore, we found that the ectopic expression of miR-124 enhanced oxidative stress and the miR-124/PTB1/PKM1/PKM2 axis constituted a feedback cascade. Finally, we showed that intratumor injection of miR-124 and siR-PTB1 induced a tumor-suppressive effect in xenografted mice. The axis was established by both in vitro and in vivo experiments to function in human colorectal cancer cells. These findings suggest that miR-124 acts as a tumor-suppressor and a modulator of energy metabolism through a PTB1/PKM1/PKM2 feedback cascade in human colorectal tumor cells.Entities:
Keywords: Colorectal cancer; PKM; PTB1; Warburg effect; miR-124
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Year: 2015 PMID: 25818238 DOI: 10.1016/j.canlet.2015.03.026
Source DB: PubMed Journal: Cancer Lett ISSN: 0304-3835 Impact factor: 8.679