SIFN-l Surpress The Proliferation Of A549Human NSCLC Cells By Down-Regulation Of Smad2

Background: As the WHO reported, in recent years lung cancer is of the highest death rate. Andalong with the worsening of the environment, the incidence is in an upward trend. Peopleurgently need to find a treatment of lung cancer with better curative effects and small side effects.sIFN-exerted a potent antitumor effect(Super interferon formerly known as freeze-driedrestructuring efficient composite interferon, because of its anticancer and antiviral effect is verygood, so the thesis commonly used sIFN-).Methods: In this study, lung cancer A549cell proliferation rate was assessed by MTT method.Compared with the same dose of ordinary interferon IFNa2b, sIFN–has a much strongerinhibition of the A549cell proliferation. Through Western blot assay and Q–PCR assay, wefound that, compared with the control, the intracellular Smad2was significantly down-regulatedby sIFN–in mRNA level and protein level. By the Dual Luciferase Reporter Assay System, wealso found the activity of Smad2promoter was sharply reduced by sIFN–. we then analysedthe DNA sequence of Smad2promoter, and found an important transcription factor ARNT(alsonamed HIF1-beta), and assayed by western blot and laser scanning confocal microscope assay.Result: Our results suggest that, compared with the control, sIFN-has a stronger effect ofARNT nuclear export and degradation in A549cell. After reduced the Smad2promoter activity,sIFN–then significantly down-regulated Smad2in mRNA level and protein level. Finally,the A549cell proliferation was strongly repressed.