Inhibition of invadopodia formation by diosgenin in tumor cells (Review)

Abstract

Diosgenin is a type of steroid extracted from the rhizome of Dioscorea plants. In traditional Chinese medicine, Dioscorea has the effect of ‘eliminating phlegm, promoting digestion, relaxing tendons, promoting blood circulation and inhibiting malaria’. Recent studies have confirmed that dios‑ genin exhibits a number of pharmacological effects, including antitumor activities. Through its antitumor effect, diosgenin is able to block tumor progression and increase the survival rate of patients with cancer; ultimately improving their quality of life. However, the mechanism underlying its pharmacological action remains unclear. Once tumor cells reach a metastatic phase, it can be fatal. Increased migration and invasiveness are the hall‑ marks of metastatic tumor cells. Invadopodia formation is key to maintaining the high migration and invasive ability of tumor cells. Invadopodia are a type of membrane structure process rich in filamentous‑actin and are common in highly invasive tumor cells. In addition to actin, numerous actin regulators, including cortical actin‑binding protein (Cortactin), accumulate in invadopodia. Cortactin is a microfilament actin‑binding protein with special repetitive domains that are directly involved in the formation of the cortical microfilament actin cell skeleton. Cortactin is also one of the main substrates of intracel‑ lular Src‑type tyrosine protein kinases and represents a highly conserved family of intracellular cortical signaling proteins. In recent years, great progress has been made in understanding the role of Cortactin and its molecular mechanism in cell motility. However, the diosgenin‑Cortactin‑invadopodia mechanism is still under investigation. Therefore, the present review focused on the current research on the regulation of invadopodia by diosgenin via Cortactin.