Triptolide inhibits migration and viability, and promotes apoptosis by targeting the PI3K/Akt signaling pathway via upregulation of miR‑125a‑5p in SW1353 human chondrosarcoma cells

Malignant chondrosarcoma is a rare type of bone cancer, for which an effective comprehensive treatment strategy is lacking. Triptolide (TPL) is an active chemical component originating from the Chinese herb Tripterygium wilfordii Hook F, which exerts inhibitory effects on various cancer cells. However, to the best of our knowledge, little is currently known about the effect of TPL on chondrosarcoma. In the present study, SW1353 human chondrosarcoma cells were used as in vitro cell model. Cell Counting Kit‑8, Annexin V/PI staining, wound healing assay, Transwell invasion assay and the detection of proinflammatory cytokines were performed to determine the effects of TPL on SW1353 chondrosarcoma cell viability, apoptosis, migration, invasion and inflammation. In addition, the protein expression levels of phosphorylated (p)‑PI3K, PI3K, p‑AKT and AKT were detected to determine whether TPL exerted its antitumor effects via the PI3K/Akt signaling pathway. Furthermore, the microRNA (miR)‑125a‑5p‑inhibitor was introduced into cells to determine whether TPL exerted its effect on SW1353 cells via miR‑125a‑5p. TPL inhibited SW1353 chondrosarcoma cell viability, migration, invasion and proinflammatory cytokine expression in a dose‑dependent manner. The most obvious effect observed in the current study was in the 50 nM TPL group. In addition, TPL inhibited PI3K/Akt signaling pathway activation and upregulated miR‑125a‑5p expression in a dose‑dependent manner. By contrast, miR‑125‑5p inhibition accelerated the viability, migration, invasion and proinflammatory cytokine expression of SW1353 cells compared with the control. Notably, miR‑125a‑5p inhibition reversed the effects of TPL on SW1353 cells. In conclusion, TPL exerted an antitumor effect on SW1353 human chondrosarcoma cells and miR‑125a‑5p served an essential role in inhibiting the tumorigenic phenotype of chondrosarcoma cells. TPL exerted its inhibitory effects on chondrosarcoma cells via upregulating miR‑125a‑5p and inhibiting the PI3K/Akt signaling pathway.