Inhibition of long non-coding RNA TSIX accelerates tibia fraction healing via binding and positively regulating the SOX6 expression.

Fragile fracture patients need to be treated with long-term fixation and the recovery process is slow. Several studies have shown that the fracture healing process is related to gene expression. We aimed to investigate the role of long chain non-coding RNA TSIX (lncRNA TSIX) on fracture healing after tibial fracture (TF) and explore the molecular mechanism underlying its action. The male C57BL/6J mice were used to construct TF models and osteoblasts were used as in vitro model. The proliferation, apoptosis, and osteogenesis-related genes of Col1a1, Col-II, and Col-X were detected to evaluate the role of lncRNA TSIX in vivo and in vitro after TF. Haematoxylin-eosin (HE) staining was conducted to confirm the fracture healing conditions. We found that LncRNA TSIX expression in plasma of TF mice significantly upregulated in a time-dependent manner. Overexpression of lncRNA TSIX could significantly inhibit proliferation but promote apoptosis and regulate the osteogenesis-related genes expression by binding and positively regulate sex-determining region Y box 6 (SOX6) expression, while knockdown of lncRNA TSIX showed the opposite effect in osteoblastic cells. Inhibition of lncRNA TSIX could improve fracture healing after TF. Taken together, our study supported that knockdown of lncRNA TSIX could promote the tibia fracture healing by binding and inhibiting the SOX6 expression. We suggest that lncRNA TSIX/SOX may be the potential targets for the treatment of TF.