RESUMO
Among the widest range of prevalent forms of cancer is oral carcinoma, which can develop anywhere in the mouth or even on the lips. Although there have been many advances in cancer treatment, the expected lifespan for OSCCs have indeed increased marginally. The load of OSCC is anticipated to increase in the near future, yet there is no sign of relief in view. Tumorigenesis is just one of the many physiological processes that can be controlled by microRNAs, a class noncoding endogenous RNAs. Several fibrosis disorders have been linked to miR- 21, and it has been utilised to distinguish oral and tongue cancer from healthy individuals. Studies empirically highlighted the significance of these transcripts as a predictor for prediction and diagnosis in OSCCs. Therefore, the present review summarizes the expression levels of miRNAs in OSCCs and evaluates their functioning in the progression or suppression of cancer. miR-21 can be considered as a prospective candidate for their translational use in OSCCs for early diagnosis prognosis surveillance and tailored treatment which should undergo further validation.
RESUMO
Chios gum mastic (CGM) is obtained from the stem and leaves of Pistacia lentiscus trees and has been extensively used for centuries in Mediterranean and Middle Eastern countries, both as a dietary supplement and herbal remedy. This study was undertaken to examine in vitro effects of cytotoxicity and growth inhibition, and the molecular mechanism underlying modulation of cell cycle and induction of apoptosis in YD9 human oral squamous carcinoma cell line treated with CGM. The viability of YD9 cells and human normal keratinocyes (HaCaT cells), and the growth inhibition of YD9 cells were assessed by the MTT assay and clonogenic assay respectively. The hoechst staining and DNA electrophoresis were conducted to observe the YD9 cells undergoing apoptosis. YD9 cells were treated with CGM, and Western blotting, immunocytochemistry, confocal microscopy and FACScan flow cytometry were conducted. Mitochondrial membrane potential change and proteasome activity were measured. CGM treatment on YD9 cells resulted in a does-dependent inhibition of cell growth and induced apoptotic cell death. And tested YD9 cells showed several lines of apoptotic manifestation. Flow cytometric analysis revealed that CGM resulted in G1 arrest in cell cycle progression which was associated with decrease in the protein expression of cyclin D1, cyclin D3, Cdk2 and Cdk4, and increase in the protein expression of p21(WAF1/CIP1) and p53. These results demonstrate that CGM induces G1 the cell cycle arrest via the modulation of cell cycle-related proteins, and apoptosis via mitochondria and caspase pathway in YD9 cells, suggesting that CGM can be considered as a novel therapeutic strategy for human oral squamous cell carcinoma from its strong cell cycle arrest and apoptosis-inducing activity.