ABSTRACT Osteosarcoma (OS) is a malignant tumor with a low survival rate and a high incidence rate worldwide. Although research has reported the involvement of long non-coding RNAs (lncRNAs) in… Click to show full abstract
ABSTRACT Osteosarcoma (OS) is a malignant tumor with a low survival rate and a high incidence rate worldwide. Although research has reported the involvement of long non-coding RNAs (lncRNAs) in the pathogenesis of OS cells, the role of TRPM2-AS, miR-15b-5p, and PPM1D in OS progression remains unclear. This study aimed to examine the interaction of the TRPM2-AS/miR-15b-5p/PPM1D axis in OS cells to gain new insights into the molecular mechanism and pathogenesis of OS. After performing in vitro functional assays, we discovered that TRPM2-AS was overexpressed in OS cells. TRPM2-AS silencing impaired OS cell viability, proliferation, and migration, while it induced apoptosis in OS cells in vitro. Our experimental analysis also revealed that PPM1D is a direct target of miR-15b-5p. TRPM2-AS silencing was found to reverse the tumorigenic effect of the miR-15b-5p inhibitor, while the miR-15b-5p inhibitor restored the inhibition of OS caused by silencing PPM1D. Moreover, our findings revealed that miR-15b-5p exerted its tumor-suppressive role by directly targeting PPM1D. In conclusion, this study suggests that TRPM2-AS could promote OS cell malignancy by sponging miR-15b-5p/PPM1D axis.
               
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