Abstract
BACKGROUND: Cullin1 is a representative member of the Cullin family, and it plays an important role in the ubiquitination of cell cycle, transcription and signal transduction related proteins. Cullin1 is closely related to the occurrence and development of a variety of malignant tumors. The aim of this study is to investigate the effects of Cullin1 on biological function of lung adenocarcinoma A549 and H1395 Cells. METHODS: The expression of Cullin1 mRNA was detected by quantitative Real-time polymerase chain reaction in lung adenocarcinoma cells (A549, H358, H1395, H1650) and human normal lung epithelial cells BEAS-2B, siRNA technology was used to interfere with lung adenocarcinoma cells with relatively high expression of Cullin1 mRNA; cell proliferation, cell cycle distribution, early cell apoptosis, invasion and migration ability were detected by methyl thiazolyl tetrazolium assay (MTT), flow cytometry and Transwell experiment; Western blot was used to detect the expression levels of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase-1 (TIMP-1), Cyclin D1, Cyclin E2, p21 and p27. RESULTS: Compared with the BEAS-2B cell, Cullin1 mRNA was highly expressed in lung adenocarcinoma cells, especially in lung adenocarcinoma A549 and H1395 cells (P<0.05). The proliferation ability of lung adenocarcinoma cells was inhibited after interference with Cullin1, and the number of cells in G1 phase increased, the number of cells in S phase decreased, and the early apoptosis rate of lung adenocarcinoma cells is significantly increased (P<0.05); The invasion and migration ability of lung adenocarcinoma cells decreased (P<0.05). After interference with Cullin1, the protein expression of MMP-9, MMP-2, CyclinD1 and CyclinE2 decreased (P<0.05), while the expression of TIMP-1, p21 and p27 protein increased (P<0.05). CONCLUSIONS: Interference with Cullin1 inhibits the proliferation, invasion and migration of lung adenocarcinoma A549 and H1395 cells, Cullin1 plays a role in promoting cancer in lung adenocarcinoma.