Abstract. Osteosarcoma is the most common type of primary bone cancer in children and adolescents, but its mechanism remains unclear. Musashi RNA-binding protein 1 (MSI1) is highly expressed in certain cancer types and functions as a putative progenitor/stem cell marker. In the present study, it was demonstrated that MSI1 expression in osteosarcoma tissue was higher compared with in the paraneoplastic tissue samples. Knockdown of MSI1 using shRNA in MG-63 and HOS cells inhibited cell proliferation in vitro and tumor formation in vivo, suggesting that MSI1 serves an essential role in osteosarcomagenesis. Further investigations demonstrated that the knockdown of MSI1 leads to the cell cycle arrest at G 0 /G 1 phase, and the upregulation of p21 and p27 protein expression in osteosarcoma cells. Additionally, luciferase assays demonstrated that MSI1 can bind to the 3' untranslated regions of p21 and p27 mRNA. In conclusion, the results of the present study suggest that the knockdown of MSI11 can suppress cell proliferation of osteosarcoma by targeting p21 and p27 and subsequently inhibiting cell cycle progression.

Diabetes mellitus adversely affects human bones and increases the risk of developing osteoporosis. In the present study, treatment with 30 mmol/l glucose was used to establish a high glucose (HG) cell model in vitro. Plasmids were used to overexpress the P2X purinoceptor 7 (P2X7) gene. Brilliant blue G and (4-benzoyl-benzoyl)-ATP were used as a P2X7 antagonist and agonist, respectively. Proliferation of osteogenic MC3T3-E1 cells and alkaline phosphatase (ALP) activity were determined using MTT and colorimetric assays, respectively. Alizarin Red S was used to assess calcification of MC3T3-E1 cells. Western blotting and reverse transcription-quantitative PCR were performed to determine protein and mRNA expression levels. The results demonstrated that HG inhibited MC3T3-E1 cell proliferation and P2X7 expression, reduced calcification, and downregulated the expression levels of ALP and osteocalcin (Ocn) in MC3T3-E1 cells. Overexpression of P2X7 in HG conditions increased calcification and proliferation, and upregulated the levels of ALP and Ocn in MC3T3-E1 cells. Inhibition of P2X7 downregulated the expressions of ALP and Ocn in MC3T3-E1 cells under HG conditions. Therefore, the present results indicated that HG caused damage to osteogenic MC3T3-E1 cells. Thus, P2X7 may be a regulatory factor that may be used to counteract the effects of HG on osteogenesis.