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ARG1 gene on proliferation and apoptosis in human embryonic kidney cell 293
Formed due to the Earth's surface and drinking water pollution in most areas of biological long-term exposure to arsenic environment and long-term low dose exposure to arsenic can lead to increased incidence of a variety of diseases and tumors, is a worldwide public health problem. Research that arsenic damage on the body from the fetal period has already begun, and will affect children's growth and will even increase morbidity and mortality in adulthood. Although arsenic is a common toxic substances, but arsenical application as a drug has 2400 years of history in recent years, studies have shown that arsenic trioxide as a new differentiation inducer, is not only safe and effective, but also in the treatment of malignant tumors, especially leukemia has great potential, further studies have shown that arsenic trioxide for other hematological malignancies and solid tumors have a good effect.The arginase gene is cloned a new gene to establish a cDNA library obtained from a human fetal brain mRNA of 4u mol / L, sodium arsenite-induced liver cancer L-02 cell lines 2 weeks, do express the spectrum of gene chip hybridization showed that the gene increased expression of known gene expression increased, suggesting that the gene cells resistant to arsenic.Arsenicals primarily through inhibition of tumor cell proliferation, promote apoptosis of tumor cell differentiation and impede tumor angiogenesis and other toxic effects of treatment of cancer. Often seen in the use of arsenical antagonism of arsenic have been found widespread antagonism of arsenic in nature, fungi, protozoa and animal cells. Arsenic resistance mechanisms on the organism is not yet very clear, mainly in the following aspects: (1) ABC membrane transporter protein superfamily member participation; (2) Glutathione and Glutathione S-transferase detoxification system; (3) of arsenic biotransformation and excretion; (4) anti-apoptotic role of apoptosis related gene expression abnormalities and changes in apoptosis-related signaling pathways; (5) arsenic resistance associated gene expression; (6) effect on the proliferation.In this study, 293 cells as a model, [Only registered users see links. ](arginase) expression plasmids and pcDNA31-ARG1 empty vector control plasmid pcDNA3.1 were transfected into 293 cells after arsenic exposure, detection ARG1 gene to gene with anti-293 cell proliferation and apoptosis of arsenic resistance. Mainly in the low arsenic concentrations NaAsO2 inhibition of cell proliferation rate, at the same time against NaAsO2 Apoptosis of 293 cells against arsenic gene in prokaryotes has been relatively clear, butEukaryotes, especially mammals and human research has just started, many of the problems is unclear, there are a lot of work worthy of further study. In addition to common cancer genes, the new arsenic-related genes such as ABCG1 and ABCA8 of the function is also actively pursued.
|293 , apoptosis , arg1 , arginase , cell , embryonic , gene , human , kidney , proliferation|
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