MicroRNA miR-23b-3p promotes osteosarcoma by targeting ventricular zone expressed PH domain-containing 1 (VEPH1)/phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway

Increasing evidence suggests that dysregulated miRNA expression can lead to the tumorigenesis of osteosarcoma (OS). Nevertheless, the potential role of miR-23b-3p in OS is unclear and remains to be explored. Microarray analysis was performed to identify key genes involved in OS. Reverse transcription quantitative polymerase chain reaction and Western blotting were used to examine miR-23b-3p expression, ventricular zone expressed PH domain-containing 1 (VEPH1) transcript (as well as other transcripts as indicated), and phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway-related protein expression. A luciferase reporter gene assay was performed to confirm the regulatory relationship between VEPH1 mRNA and miR-23b-3p. Cell viability was evaluated using the Cell Counting Kit-8 assay, cell growth was assessed using the bromodeoxyuridine enzyme-linked immunosorbent assay, and cell migration was tested using a wound healing assay. We found significant upregulation of miR-23b-3p in OS, which prominently promoted the viability, proliferation, and migration of OS cells. Additionally, VEPH1 was found to be a target of miR-23b-3p and its expression was decreased in OS. Lastly, VEPH1 alleviated the promotion effect of miR-23b-3p on the malignancy phenotypes of OS cells via the PI3K/AKT signaling pathway. Thus, miR-23b-3p augmented the viability, proliferation, and migration of OS cells by directly targeting and downregulating VEPH1, which inhibited the activation of the PI3K/AKT signaling pathway.

Automated summary

Studies have shown that upregulation of miR-23b-3p in osteosarcoma promotes cell proliferation, migration, and viability. VEPH1, a target of miR-23b-3p, attenuates the malignancy effects of miRNA on osteosarcoma cells by inhibiting the PI3K/AKT signaling pathway.