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Green Wave- in the Prevention and Treatment of Oral Cancer -- Quercetin
Jul 31, 2018

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Quercetin is also known as quercetin and quercetin, and quercetin and its derivatives are one of the most common flavonoid substances in dietary ingredients. The molecular formula is C15H10O7. It is an effective component of some Chinese herbal medicines such as 37, rutin and apocynum, and is widely used in a variety of foods. It is a very strong natural antioxidant. It has many biological activities, such as removing free radicals, inhibiting inflammatory reaction, anti thrombosis, antivirus, anti-cancer, anti-cancer, anti infection, immunosuppression, cardiovascular protection and blood glucose regulation. With the development of "green wave" era, the quercetin from natural plants is becoming more and more important. Research hot spots at home and abroad.


The incidence of oral cancer in the world is increasing year by year. Oral cancer occurs mostly in buccal mucosa, upper and lower gums, hard palate, tongue and bottom of mouth. Oral cancer accounts for 1.9%-3.5% of malignant tumor of the whole body, which is 4.7%-20.3% in head and neck cancer, second only to nasopharyngeal carcinoma, the second place in maxillofacial malignant tumor, easy to transfer. And the prognosis is not optimistic. The main means of treatment include surgery, radiotherapy and chemotherapy.

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Some recent studies have confirmed that quercetin can induce apoptosis in many human tumor cells, but it has little effect on normal tissue cells, such as liver cancer, lung cancer, breast cancer, bladder cancer, ovarian cancer, and gastric cancer. Quercetin can inhibit the growth and proliferation of cancer cells, and also has the effect of reversing multidrug resistance. Combined with other anticancer drugs can also enhance the role of anticancer drugs, but the role in oral cancer cells has not been confirmed.


Recently, a report published by Chinese researchers confirmed that quercetin can induce apoptosis in human oral cancer cells. The study used quercetin treatment for 6 to 48 hours with flow cytometry, iodized / propionate iodide (PI) double staining, protein immunoblotting, confocal laser and other techniques. The results showed that the apoptosis rate of oral cancer cells increased after continuous quercetin treatment, the increase of calcium isolated products and reactive oxygen species, mitochondrial membrane. The level of potential decreased, the apoptotic products increased and the levels of apoptosis related proteins increased. 


The results of protein immunoblotting showed that quercetin increased fatty acid synthetase, fatty acid synthetase ligand, Fas dead domain related protein and apoptotic protease -8, all of which were associated with cell apoptosis. And quercetin increased the level of transcription factor (ATF) -6 alpha, ATF-6 beta and gastrin releasing peptide, increased the level of apoptotic protein BH3, and reduced the level of B cell lymphoma factor 2 and B cell lymphoma factor -XL. In addition, confocal experiments showed that quercetin could increase the expression levels of cytochrome C, apoptosis inducing factor and endonuclease G. These findings suggest that quercetin may become an effective treatment for oral cancer in the future.


Quercetin-rich foods, such as vegetables such as onions and fruits such as apples, tea and wine, can be eaten appropriately in daily life to prevent oral cancer. At present, the study of quercetin is mainly focused on the preclinical stage. It is not fully understood whether the effect of quercetin has the same effect. Therefore, it is necessary to study the biological effects of quercetin more deeply and carry out the experiment to lay the foundation for its clinical treatment. The other problem is that quercetin is difficult to dissolve in water and has low oral utilization. The new dosage forms include quercetin solid lipid nanoparticles and microemulsion system, and the study of dosage forms also has a lot of space.


References: 

Ma YS, Yao CN, Liu HC, et al.Q uercetin induced apoptosis of human oral cancer SAS cells through mitochondria and endoplasmic reticulum mediated signaling pathways. Oncol Lett. 2018, 15(6):9663-9672.


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