Effect Of SCIN In Proliferation Of Non-small Cell Lung Cancer

Objective:Aberration of cell proliferation is considered to be the main cause of non-small cell lung cancer(NSCLC). SCIN is an important actin-binding protein. As a regulon of F-actin, multitude complex functions of SCIN have been found. In addition to its role in actin filament remodeling, SCIN has some roles in several cellular processes, including cell exocytosis, differentiation, motility and so on, SCIN also plays a pivotal role in tumorigenesis possibly. The aim of current study is to confirm that SCIN would play an important role in proliferation of NSCLC cells, which would provide scientific basis for a further understanding of the molecular mechanisms in tumorigenesis of NSCLC.Methods:1. By immunochemical ABC techenique, we detected the expression of SCIN in the pathological paraffin tissues of NSCLC and]inflammatory pseudotumors, then analyzed the association between them by SPSS software.2. Expression of SCIN in nine NSCLC cell lines was measured by western blotting.3. Construction of SCIN-shRNA lentiviral vector.4. A549cell line was transfected by SCIN-shRNA lentiviral vector, RT-PCR and western blotting were performed to detect the expressions of SCIN.5. Alterations of NSCLC cells biological behaviors were analyzed by MTS assay, cell growth curve experiment, flow cytometry cell cycle analysis. 6. In vivo studies of the relation of SCIN and the proliferation of NSCLC cells.7. RT-PCR analyzed the target genes after knockdown SCIN.Results:1. The expression of SCIN is mainly in cytoplasm, and positive rate in NSCLC was significantly higher than inflammation tissues (P<0.05).2. Western blotting detected that SCIN was expressed in all nine NSCLC cell lines, and A549cell line was chosen as experimental model.3. Western blotting and RT-PCR confirm that SCIN-shRNA lentiviral vector could decrease the expression of SCIN.4. MTS assay and cell growth curve experiment showed that the proliferation of A549cells were suppressed, flow cytometry cell cycle analysis results revealed significant G1arrest in cell cycle in SCIN-knockdown A549cell model.5. The average volume of turner in the group of SCIN-shRNA is smaller than the group of control.6. RT-PCR results revealed that CDK2was decrease after knockdowning SCIN.Conclusions:1. SCIN might participate in the progression of NSCLC mediated by CDK2.2. The expression of SCIN is higher in the issues of NSCLC than in inflammation.