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 effec‑ tive treatment for chondrosarcoma, it has low efficacy in the metastasis stage. Antrodia cinnamomea 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 regula‑ tion 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 chondrosar‑ coma 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 overex‑ pression of MMP‑7 antagonized antcin K‑induced inhibition of cell migration and invasion. Antcin K abolished the activa‑ tion 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.