| Background：Lung cancer is one of the leading causes of cancer deaths in the world. It canbe divided into small-cell lung cancer (SCLC) and non-small-cell lung cancer(NSCLC). NSCLC,which originates from the lung epithelial cells, is comprised ofvarious histological subtypes including such as adenocarcinoma, bronchioloalveolar,squamous, anaplastic and large-cell carcinomas. It’s well known that invasion andmetastasis is one of the leading causes of death among patients with cancers. Therehas been considerable progress in understanding mechanism of lung cancer. However,many details of genetic cause remain elusive. Previous studies had shown thatP38MAPK signal pathway was involved into the development and progression ofcancer invasion and metastasis. Also EMT and MMPs had been proved to play thevery important roles in the invasion and metastasis of cancers. It had been shown thatP38MAPK signal pathway had significant influence to some EMT-related proteins，aswell as to some of MMPs. The aim of this study was to find out if P38MAPK signalpathway regulated the invasion and metastasis of NSCLC through EMT-relatedproteins or MMPs.Method：The activity of P38were inhibited by the P38inhibitors SB203580andSB239063. Wound healing assay and Transwell assay were the common way todetect the ability of cell migration and invasion. The activity of MMP9was detectedby Zymographic analysis. All the expression of proteins were detected byWestern-blot.Result：The ability of cell migration and invasion had been inhibited by after the activity of P38was inhibited by the P38inhibitor：SB203580and SB239063. Theexpressions of EMT-related proteins:β-catenin,Vimentin and snail were changed afterinhibiting the phosphorylation of P38. While the activity of MMP9had no changeafter both SB203580and SB239063were used, as well as the expression of MMP9protein.Conclusion：P38regulated the invasion and metastasis of NSCLC through EMT-relatedproteins. MMP9was not involved into the P38-related invasion and metastasis ofNSCLC.
|
PDF Full Text Request