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

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.