Related Experiment Video
Updated: Jan 24, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
Published on: June 3, 2018
miR-23b-3p suppressing PGC1α promotes proliferation through reprogramming metabolism in osteosarcoma
Ran Zhu1, Xinpan Li2, Yanhong Ma3
1Department of Rehabilitation Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Abstract:
Metabolic shift from oxidative phosphorylation (OXPHOS) to glycolysis is a hallmark of osteosarcoma (OS). However, the mechanisms of the metabolic switch have not been completely elucidated. Here we reported that the miR-23b-3p was significantly upregulated in OS cells. Functional studies suggested that knockdown of miR-23b-3p could inhibit OS cell proliferation in vitro or in vivo. In addition, suppression of miR-23b-3p could lead to upregulation of OXPHOS and suppression of glycolysis. Mechanistically, miR-23b-3p promoted OS cell proliferation and inhibited OXPHOS in OS, at least in part, by directly targeting peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC1α) and inhibiting its expression. Our data highlights important roles of miR-23b-3p and PGC1α in glucose metabolism reprogram of OS. The suppression of miR-23b-3p may provide effective therapeutic strategies for the treatment of OS.
Related Concept Videos
What is Metabolism?
The Eukaryotic Promoter Region
The Eukaryotic Promoter Region
Abnormal Proliferation
Introduction to Nuclear Reprogramming
Methods of Nuclear Reprogramming

