[Study of Mechanism of Esophageal Cancer Development through MKK6 Over-expression Regulated SIRTI Expression Level].

免疫印迹 细胞凋亡 流式细胞术 食管癌 细胞生长 活力测定 p38丝裂原活化蛋白激酶 调节器 表达式向量 细胞 污渍 化学 MAPK/ERK通路 分子生物学 生物 信号转导 细胞生物学 癌症 内科学 重组DNA 医学 基因 生物化学
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期刊:PubMed 卷期号:46 (4): 548-53
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To observe the influence of silent information regulator of transcription 1 (SIRT1) level by regulation of MKK6 over-expression in esophageal cancer cell Eca109, and then to explore the relationship between p38-MAPK-SIRT1 axis and progressing of esophageal cancer.MKK6 over-expression vector was successfully constructed firstly. Then the divided Eca109 cells were treated according to four groups: empty vector group, MKK6 over-xpression group (MKK6 group), MKK6-SIRT1 ShRNA group, MKK6-RES group. The expression of MKK6 and endogenous SIRT1 were tested by Western blot; cell proliferation capability was detected by MTT method; cell invasion force was observed by transwell method; and cell apoptosis was detected with flow cytometry.pcDNA3.1 (+)/myc-His A-MKK6 over-expression vector was constructed successfully and proved by sequencing. MKK6's over-expressing could reduce the expression of endogenous SIRT1. The viability of Eca109 cells was decreased. The increasing of invasion and apoptosis was observed.There might be the p38-MAPK-SIRT1 regulation axis in Eca109 cells and affecting on a series of physiological characteristics of Eca109 cells.

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