Background
Osteosarcoma (OS) is a common tumor of bone, and the high incidence and poor prognosis of OS call for novel therapeutic strategies. We aimed to explore the functional role of lentinan (LNT) in human OS MG63 cells as well as the underlying mechanisms.
Conclusion
LNT reduced proliferation and induced apoptosis and autophagy by up-regulating miR-340 in MG63 cells, along with inhibition of the MAPK/ERK pathway.
Methods
Cell viability of MG63 cells under LNT stimulation was measured by CCK-8 assay to explore the adequate concentration of LNT. Cell proliferation, apoptosis and expression of microRNA (miR)-340 in MG63 cells after LNT treatments were assayed by BrdU incorporation assay, flow cytometry assay and quantitative reverse transcription PCR, respectively. Expression of proteins associated with cell cycle, apoptosis, and autophagy were determined by western blot analysis. Subsequently, whether LNT affected MG63 cells through miR-340 as well as the related signaling pathway was explored.
Results
Cell viability was reduced by 5-100 mg/mL of LNT. Percentage of BrdU-positive cells was reduced while that of apoptotic cells was enhanced by LNT treatment. LNT decreased cyclin D1 level but increased levels of active caspase-3 and caspase-9. After treatment, LNT enhanced LC3B-II/LC3B-I and Beclin-1 levels but reduced the p62 level. The miR-340 level was up-regulated by LNT, and further experiments showed LNT promoted apoptosis and autophagy through up-regulating miR-340. Moreover, LNT reduced the phosphorylated levels of MAPK and ERK through up-regulating miR-340.