Menadione (Vitamin K3) Induces Apoptosis of Human Oral Cancer Cells and Reduces their Metastatic Potential by Modulating the Expression of Epithelial to Mesenchymal Transition Markers and Inhibiting Migration

Abstract

Oral cancer is one of the most commonly occurring cancers worldwide, decreasing the patient’s survival ratedue to tumor recurrence and metastasis. Menadione (Vitamin K3) is known to exhibit cytotoxicity in variouscancer cells but the present study focused on its effects on viability, apoptosis, epithelial to mesenchymal transition(EMT), anchorage independent growth and migration of oral cancer cells. The results show that menadioneis more cytotoxic to SAS (oral squamous carcinoma) cells but not to non-tumorigenic HEK293 and HaCaTcells. Menadione treatment increased the expression of pro-apoptotic proteins, Bax and p53, with a concurrentdecrease in anti-apoptotic proteins, Bcl-2 and p65. Menadione induced the expression of E-cadherin but reducedthe expression of EMT markers, vimentin and fibronectin. Menadione also inhibited anchorage independentgrowth and migration in SAS cells. These findings reveal and confirm that menadione is a potential candidate inoral cancer therapy as it exhibits cytotoxic, antineoplastic and antimigratory effects besides effectively blockingEMT in oral cancer cells.

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