Piceatannol suppresses proliferation and induces apoptosis by regulation of the microRNA‑21/phosphatase and tensin homolog/protein kinase B signaling pathway in osteosarcoma cells.

Abstract

Piceatannol (Pice), a natural analog of resveratrol, has been identified as an anticancer agent in various cancers by modulating the expression of microRNAs (miRNAs/miRs). However, the molecular mechanisms underlying the anticancer effects of Pice in osteosarcoma (OS) cells remain unclear. Thus, we hypothesized that Pice exerts anticancer effects on OS cells via the regulation of miRNA expression. Herein, we performed a MTT assay and flow cytometric analysis to determine cell viability and apoptosis in OS cells treated with Pice, respectively. Our results showed that Pice inhibits proliferation in a dose-dependent manner induces the apoptosis of OS cells. More importantly, miRNA microarray analysis identified that Pice alters miRNA expression profiles in human OS cells after treatment with Pice, and miR-21 was the most significantly downregulated. In addition, the therapeutic effects of Pice on OS cells were weakened by restoration of miR-21. In addition, we further verified that phosphatase and tensin homolog (PTEN), a tumor suppressor gene, is the functional target of miR-21 and Pice blocks the PTEN/AKT signaling pathway through inhibiting miR-21 expression in OS cells. Our findings suggested that Pice may exert anticancer effects on OS cells via mediating the miR-21/PTEN/AKT signaling pathway and could be considered to be a potential anticancer agent for treating OS.