Convallatoxin inhibits proliferation and angiogenesis of glioma cells via regulating JAK/STAT3 pathway.

Abstract

Gliomas can cause nerve cancer-related death, and surgical removal can be challenging. Convallatoxin functioned as anti-proliferation and anti-angiogenesis in cancer cells. However, convallatoxin's effect on glioma remains unclear. The aim of this study is to investigate the effect of convallatoxin on the proliferation and angiogenesis of glioma cells, and explore the underlying mechanism. Human glioma cell lines U251MG and A172 were treated with 12.5, 25, and 50 nM convallatoxin. Cell proliferation was investigated using the CCK-8 assay and colony formation assay. Migration and invasion were analyzed with transwell assays. Angiogenesis was evaluated using a tube formation assay. The phosphorylation of Janus kinase (JAK) and signal transducer and activator of transcription 3 (STAT3) was measured using Western blots. A xenotransplantation model of nude mice was used to investigate glioma progression. In U251MG and A172 cells, convallatoxin dose-dependently reduced cell viability and colony formation. Convallatoxin suppressed migration and invasion. Similarly, convallatoxin-treated cells had weakened angiogenesis. Convallatoxin downregulated JAK and STAT3 phosphorylation levels. Convallatoxin also inhibited glioma progression in nude mice xenotransplantation models. By inhibiting the JAK/STAT3 signaling pathway, convallatoxin inhibited proliferation, migration, invasion, and angiogenesis of glioma cells, proving to be a promising therapeutic candidate for gliomas.