Silencing of lncRNA KLF3‐AS1 represses cell growth in osteosarcoma via miR‐338‐3p/MEF2C axis

BACKGROUND: Osteosarcoma (OS) is a highly recurrent malignancy occurring among adolescents. The goal of this research was to scrutinize the role and action mechanism of KLF3‐AS1 in OS. METHODS: Western blotting and quantitative reverse transcription real‐time PCR were conducted to ascertain the mRNA expressions of miR‐338‐3p, KLF3‐AS1, and MEF2C in OS cell lines and tissue samples. Colony formation and CCK‐8 experiments were done to evaluate the proliferative capacity of the cells. Western blotting was also executed to measure the relative expressions of the proteins Bcl‐2 and Bax. RNA immunoprecipitation and dual luciferase reporter experiments were carried out to validate the target relationships among MEF2C, KLF3‐AS1, and miR‐338‐3p. Mouse xenograft models were created to assess the influences of KLF3‐AS1 on the growth of tumors in vivo. RESULTS: Elevated levels of KLF3‐AS1 and MEF2C and reduced amounts of miR‐338‐3p were identified in OS. KLF3‐AS1 targeted miR‐338‐3p, and miR‐338‐3p further targeted MEF2C. Silencing KLF3‐AS1 induced apoptosis and attenuated proliferation in vitro and repressed the tumor growth in vivo. Inhibiting miR‐338‐3p inverted the cancer‐suppressing effects of KLF3‐AS1 silencing. Meanwhile, loss of MEF2C partially eliminated the effects brought about by miR‐338‐3p downregulation, namely the stimulation of cell growth and suppression of apoptosis. CONCLUSIONS: Silencing of KLF3‐AS1 could repress the growth of cells and induce apoptosis by regulating miR‐338‐3p/MEF2C in OS. This suggests that the regulatory axis KLF3‐AS1/miR‐338‐3p/MEF2C is a prospective target for OS treatment.