Aims To establish the methods of primary culture of fibroblast-like synoviocytes in rats with adju-vant arthritis(AA-FLS)and analyze the feature and to investigate the possibility of AA-FLS as the model for the RA in vitro.Methods The synovial cells obtained from the SD rats were immunized by the Mtb and iden-tified by morphology and immunocytochemistry.The viability of AA-FLS was assessed by Cell Counting Kit-8.ELISA was applied to detect TNF-αand IL-1 βin cell media. Apoptosis was measured by Hochest 33258.The expressions of mitochondrial apoptosis-re-lated molecules,including Bcl-2,Bax,Pro-caspase-3 and Cleave-caspase-3 were determined by Western Blot.Result In isolated primary synovial cells,more
than 95% of AA-FLSs were fusiform.Immunocyto-chemistry result showed a positive expression of vimen-tin and a negative expression of CD68 in AA-FLS.Cell proliferation of AA-FLS was higher than FLS and cell apoptosis of AA-FLS was curbed.Western blot data demonstrated that the protein expressions of Bcl-2,Bax were regulated and the expression of caspase-3 was ac-tivated in AA-FLS.Conclusions AA-FLS is biologi-cally characterized by high level proliferation activity and inflammatory cytokines and apoptosis suppression. AA-FLS can be used as the model for the RA in vitro.

Metastasis is crucial for the mortality of non-small cell lung carcinoma (NSCLC) patients. The epithelial-mesenchymal transition (EMT) plays a critical role in regulating tumor metastasis. Glioma-associated oncogene 1 (Gli1) is aberrantly active in a series of tumor tissues. However, the molecular regulatory relationships between Gli1 and NSCLC metastasis have not yet been identified. Herein, we reported Gli1 promoted NSCLC metastasis. High Gli1 expression was associated with poor survival of NSCLC patients. Ectopic expression of Gli1 in low metastatic A549 and NCI-H460 cells enhanced their migration, invasion abilities and facilitated EMT process, whereas knock-down of Gli1 in high metastatic NCI-H1299 and NCI-H1703 cells showed an opposite effect. Notably, Gli1 overexpression accelerated the lung and liver metastasis of NSCLC in the intravenously injected metastasis model. Further research showed that Gli1 positively regulated Snail expression by binding to its promoter and enhancing its protein stability, thereby facilitating the migration, invasion and EMT of NSCLC. In addition, administration of GANT-61, a Gli1 inhibitor, obviously suppressed the metastasis of NSCLC. Collectively, our study reveals that Gli1 is a critical regulator for NSCLC metastasis and suggests that targeting Gli1 is a prospective therapy strategy for metastatic NSCLC.