Abstract
Conventional therapeutic processes in patient with OSCC are associated with several unfavorable effects leading to patients with poor survival rate. Metformin has been shown to protect against a variety of specific diseases, including cancer. However, the precise roles and mechanisms underlying the therapeutic effects of metformin on OSCC remain elusive. In the current study, in vitro and xenograft model experiments revealed that metformin inhibited growth and metastasis of oral cancer cells. Importantly, metformin-restrained tumorigenesis of oral cancer was accompanied with strong decrease of both Aurora-A and Late SV40 Factor (LSF) expressions. Furthermore, LSF contributed to Aurora-A-elicited malignancy behaviors of oral cancer via binding to the promoter region of Aurora-A. A significant correlation was observed between LSF and Aurora-A levels in a cohort of specimens of oral cancer. These findings showed that a novel LSF/Aurora-A-signaling inhibition supports the rationale of using metformin as potential OSCC therapeutics.
Highlights
Oral squamous cell carcinoma (OSCC) is a common malignancy in South-East Asia and India
To evaluate if the inhibition of oral cancer cell growth by metformin was mediated through cell cycle arrest, FACS analysis of DNA content was performed on 3 cell lines treated with increasing doses of metformin (5 to 10 mM) for 48 hours
FACScan analysis showed that the distribution of cell cycle of oral cancer cells treated with metformin was not alteration, compared to control group (Fig. 1E)
Summary
Oral squamous cell carcinoma (OSCC) is a common malignancy in South-East Asia and India. Despite the recent advances in technology and multidisciplinary intervention, only modest improvements in the survival of oral cancer have been achieved and these are attributed mainly to diagnosis at an early stage, rather than to therapeutic interventions[1]. This means that standard treatment fails in a significant proportion of patients and salvage surgery is unsatisfactory, it depends on the stage of the recurrent tumor[2]. Recent in vitro experiments reported that metformin may be through AMPK-independent mechanisms to suppress tumor growth[9] These studies point out that metformin may evoke a variety of signaling to prevent cancer development. The effect of metformin to LSF expression in oral cancer is still unclear
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