Oral and pharyngeal cancer is the most common malignant human cancers. Chemotherapy is an effective approach for anti-oral cancer therapy, while the drug tolerance and resistance remain a problem for oral cancer patients. Aloe-emodin, rhein and physcion are classified as anthraquinones, which are the main pharmacodynamic ingredients of Rheum undulatum L.. This study was undertaken to investigate whether aloe-emodin, rhein and physcion show inhibiting growth and inducing apoptosis in oral squamous cell carcinoma SCC15 cells. We found that aloe-emodin show inhibiting growth and inducing apoptosis in oral squamous cell carcinoma SCC15 cells, we also investigated the underlying mechanisms of apoptosis induced by aloe-emodin. Thiazolyl blue tetrazolium bromide (MTT) test was used to detect cell proliferation. Cell apoptosis was detected by flow cytometry. We also used western blot analysis to detect the potential mechanisms of apoptosis. Aloe-emodin, rhein and physcion inhibit the proliferation of SCC15 cells and the order of inhibition level are aloe-emodin > Rhein > Physcion, the half maximal inhibitory concentrations (IC50) value of aloe-emodin was 60.90 μM at 48 h of treatment. Aloe-emodin treatment resulted in a time- and dose-dependent decrease in cell viability and increased the apoptotic cell ratio. The results of western blotting showed the expression levels of caspase-9 and caspase-3 proteins increased following aloe-emodin treatment. Our results revealed that aloe-emodin treatment could inhibit cell viability of SCC15 cells and the potential mechanism of inhibition might be through the induction of apoptosis by regulation of the expression levels of caspase-9 and caspase-3. This indicates that aloe-emodin may be a good agent for anti-oral cancer drug exploring.

Oral squamous cell carcinoma (OSCC) is one of the common malignant tumors in the head and neck, characterized by high malignancy, rapid growth and metastasis, high invasive ability, and high mortality. In recent years, surgery combined with chemotherapy or radiotherapy remains the preferred clinical treatment for OSCC, despite considerable advances in diagnostic and therapeutic techniques. Hence, new targeted therapy is urgently needed. Histone modification affects the function of massive cells through histone acetyltransferase and histone deacetylase. Accompanied by the progress of some diseases, especially tumors, these proteins often show abnormal functions, and by reversing these abnormalities with drugs or gene therapy, the cancer phenotype can even be restored to normal. As a result, they are potential drug targets. This article reviewed the role of the histone dynamic process of acetylation modifications and their associated active modifying enzymes in the pathogenesis and progress of OSCC. Moreover, we explored the value of histone acetylation modification as a potential therapeutic target and the new progress of related drugs in clinical treatment.