Molecular mechanism of allicin-induced apoptosis in human oral squamous cell carcinoma (OSCC)

Abstract

90% - 95% of oral malignancies are reported to be contributed by oral squamous cell carcinoma (OSCC). Patients with oral cancer also have suffered from a stagnant survival rate of 50% for decades. With the advancement in technologies and medicine discovery, the standard solution for oral cancer is via chemotherapy and surgery. An alternative for the treatment is by incorporating a genotoxic drug, cisplatin. Unfortunately, cisplatin has been reported by many patients to give unpleasant effects such as nausea, vomiting, diarrhea and abdominal pain. Hence, a more reliable treatment needs to be unleashed. Allicin (diallylthiosulfinate) is well known for its antioxidant, antifungal, anti-inflammatory and antimicrobial purposes. Numerous studies have also reported the effectiveness of allicin as an anticancer agent against multiple cancer cell strains. With treatment of allicin in a dose-dependent manner, inhibition of carcinoma cells proliferation through a programmed cell death called apoptosis was considered favourable. Allicin induces apoptosis by activating cascades of caspases and caspase independent pathways as well as increasing p53 and Bax/Bcl2 expression. Allicin serves many potentials to fight off oral cancer carcinoma cells but there seems to be a limited amount of study in the oral cancer area. Therefore, this review article would like to highlight the reported studies on allicin in various cancer cell lines including oral cancer cells.