Antcin K inhibits chondrosarcoma motility by reducing MMP‑7 expression via downregulation of the PI3K, Akt, mTOR and NF‑κB signaling pathway.

Chondrosarcoma is the second most common form of primary bone cancer originating from cartilage. Chondrosarcoma cells have a high propensity to spread to other organs during the advanced stage, with the lung being a preferred site. Although surgery is the most effective treatment for chondrosarcoma, it has low efficacy in the metastasis stage. is the source of the triterpenoid antcin K, which exhibits immunomodulatory and anti‑inflammatory properties. However, the therapeutic function of antcin K on chondrosarcoma has not yet been elucidated. The inhibitory effect of antcin K was evaluated using migration and invasion assays while cell toxicity was determined using the MTT assay. Molecular function regulation by antcin K was investigated by RNA sequencing and Ingenuity Pathway Analysis. The present study revealed that antcin K decreases migration and invasion in two chondrosarcoma cell lines. RNA sequencing revealed that MMP‑7 serves a key role in antcin K‑mediated motility of chondrosarcoma cells. Antcin K diminished MMP‑7 expression, and overexpression of MMP‑7 antagonized antcin K‑induced inhibition of cell migration and invasion. Antcin K abolished the activation of PI3K, Akt, mTOR and NF‑κB pathways. The present study demonstrated that antcin K is a novel candidate for chondrosarcoma motility inhibition by decreasing the PI3K, Akt, mTOR and NF‑κB signaling cascades, which inhibits MMP‑7 production.