18β -glycyrrhetinic acid inhibited the proliferation of human colon cancer HT29 cell research.docVIP

18β -glycyrrhetinic acid inhibited the proliferation of human colon cancer HT29 cell research.doc

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18β -glycyrrhetinic acid inhibited the proliferation of human colon cancer HT29 cell research

 PAGE \* MERGEFORMAT 5 18β -glycyrrhetinic acid inhibited the proliferation of human colon cancer HT29 cell research [Abstract] Objective To observe the 18β -glycyrrhetinic acid (18β -glycyrrhetinic acid, GA) on human colon cancer HT29 cell proliferation, and from the cell cycle and cyclin-dependent kinase inhibitor (p16, p21, p27) expression in Feng degree to explore possible mechanisms. Approach to the role of different concentrations of GA colon cancer HT29 cells, MTT assay (MTT) cell proliferation detected by flow cytometry cell cycle, Western blot to detect cyclin-dependent kinase inhibitor (p16, p21 , p27) changes. GA effect the results of HT29 cells, proliferation was inhibited. GA treatment group cells were arrested at the G1 / S phase, and the emergence of p16, p21, p27 protein levels increase. Conclusion GA inhibit proliferation of human colon cancer cells, its mechanism and increase p16, p21, p27 proteins are involved. [Keywords:] 18β -glycyrrhetinic acid colon tumor cell cycle p16 p21 p27 Abstract: ObjectiveTo observe the effects of 18β -glycyrrhetinic acid (GA) on proliferation, cell cycle and expression of CKIs of human colon carcinoma cell line HT29, and to investigate the mechanism of GA on colon cancer cell. MethodsAfter HT29 cells treated with varible dose of GA, we detectd the proliferation by MTT, and observed cell cycle by flow cytometer, and studied the protein level of CKIs (p16, p21, p27) with Western blot. ResultsGA could inhibit the proliferation of HT29 cell, and cause G1 phase arrest . The protein of p16, p21 and p27 of cancer cells treated with GA were up-regulated in dose-and time-dependent manner. ConclusionGA could inhibit proliferation and induce differentiation in human colon cancer cell line HT29 through up-regulating the expression of CKIs , especially p16, p21 and p27. Keywords:: 18β -glycyrrhetinic acid; Colon cancer; Cell cycle cyclin-dependent kinase inhibitors (CKIs); p16; p21; p27 18β -glycyrrhetinic acid (18β -g

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