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All-trans Retinal Acid(ATRA) Inhibits The Proliferation Of Colonal Cancer Through Extracellular Signal Regulated Kinase(ERK1/2) Signal Pathway

Posted on:2012-12-26Degree:MasterType:Thesis
Country:ChinaCandidate:Y ChenFull Text:PDF
GTID:2154330335977047Subject:Pathology and pathophysiology
Abstract/Summary:PDF Full Text Request
Background and Purposes:Colonal cancer is a common digestive tract malignant tumor,almost 50% are relevant with a genetic mutation in the ras. Numerous studies show that Ras-MEK1/2-ERK1/2 signaling are abnormal activated during the develop- ment and metastasis of a variety of tumor(include colonal cancer). Retinoic acid belongs to the family of Vitamin A, with the different COOH direction which are divided into two isomers, that is all-trans retinoic acid (ATRA) and cis-retinoic acid. Cell differentiation or growth inhibition of a lot of tumor can be induced by ATRA. Therefore this study was to illustrate whether the growth of colonal cancer cells are suppressed through extracellular signal regulated kinase (ERK1/2) signal pathway in response to all-trans retinoic acid (ATRA) treatment.Method:We observed the proliferation of the LS174Tcolonal cancer cells by MTT assay; The expression of MEK/ERK in LS174T colonal cancer cell after the treatment of ATRA are detected with RT-PCR and Western blots. With ATRA, PD98059 (the specific inhibitor of MEK1/2) supplement ATRA, we observed the proliferation and apoptosis of the LS174Tcolonal cancer cells by flow cytometric analysis.Result:After the treatment of ATRA, the LS174T colonal cancer cell proliferation was inhibited, during the experiment the expression level of MEK/ERK and the phosphorylation level of ERK are all increased in LS174T cancer cell.PD98059 inhibits the phosphorylation level of ERK induced by ATRA partly. Through the analysis of flow cytometric, the apoptosis of tumor cells are significantly higher by the combination of PD98059 and ATRA than by ATRA.Conclusion:ATRA inhibits the proliferation of colonal cancer cell,and induces the apoptosis of cancer cells which may be mediated besides MEK/ERK signal pathway.
Keywords/Search Tags:ATRA, ERK, PD98059, colonal tumor
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