ALKBH5/YTHDF2 Axis Regulates Osteogenic Differentiation Through Mediating the m6A Modification of ELK1
Huan Yu, Ting Ruan, Yongxing Peng
TL;DR
This study explores how m6A methylation affects bone formation in osteoporosis, identifying a key pathway involving ALKBH5, YTHDF2, and ELK1.
Contribution
The study identifies a novel regulatory axis involving ALKBH5, YTHDF2, and ELK1 in osteogenic differentiation during osteoporosis.
Findings
ALKBH5 is downregulated in osteoporosis and suppresses osteogenic differentiation.
YTHDF2 acts as an m6A reader for ALKBH5-mediated demethylation of ELK1 mRNA.
ALKBH5/YTHDF2 axis regulates bone formation through ELK1, offering a potential therapeutic target for osteoporosis.
Abstract
This study aimed to investigate the role of N6‐methyladenosine (m6A) methylation in osteogenic differentiation during osteoporosis (OP). Serum specimens were obtained from 25 individuals diagnosed with OP and 25 age‐matched healthy controls. In parallel, MC3T3‐E1 preosteoblastic cells were employed for in vitro functional assays. Expression levels of m6A‐associated genes were quantified using qPCR. Osteogenic potential was evaluated by measuring ALP activity with an ALP assay kit and by assessing matrix mineralization through Alizarin Red S staining. RIP and dual‐luciferase reporter assays were performed to elucidate the molecular interactions involved. To corroborate the in vitro observations, an ovariectomized (OVX) mouse model of OP was established for in vivo validation. The results revealed a significant downregulation of AlkB Homolog 5 (ALKBH5) in both serum samples from OP…
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Taxonomy
TopicsRNA modifications and cancer · Cancer-related gene regulation · Kruppel-like factors research