D Wang1, Z-M Gao, L-G Han, F Xu, K Liu, Y Shen. 1. Department of Thoracic Surgery, Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China. qdsheny163.com.
Abstract
OBJECTIVE: Recently, long non-coding RNAs (lncRNAs) have caught more attention for their role in tumor progression. Lung adenocarcinoma (LAC) is one of these ordinary malignant tumors. This study aims to identify whether lncRNA CASC2 (cancer susceptibility candidate 2) can regulate the metastasis of LAC, and find out its potential mechanism. PATIENTS AND METHODS: RT-qPCR was conducted to detect CASC2 expression level in 63 LAC tissues and 4 LAC cells. Besides, statistical methods were applied to analyze clinical data and prognosis in the 63 patients. Furthermore, function experiments were performed to determine the effect of CASC2 on LAC metastasis in vitro. The potential mechanism was further explored by RT-qPCR and Western blot assay. RESULTS: In our study, CASC2 expression level was lower in LAC tissues than that in corresponding tissues. CASC2 expression was associated with lymph node metastasis, clinical stage and survival time of these patients. Moreover, overexpression of CASC2 inhibited migrated and invaded ability of LAC cells. Then, epithelial to mesenchymal transition (EMT) process of LAC cells and SOX4 expression was suppressed by upregulating CASC2. CONCLUSIONS: These results indicate that CASC2 could inhibit metastasis and EMT of LAC via suppressing SOX4, which may offer a new vision for interpreting the mechanism of LAC metastasis.
OBJECTIVE: Recently, long non-coding RNAs (lncRNAs) have caught more attention for their role in tumor progression. Lung adenocarcinoma (LAC) is one of these ordinary malignant tumors. This study aims to identify whether lncRNA CASC2 (cancer susceptibility candidate 2) can regulate the metastasis of LAC, and find out its potential mechanism. PATIENTS AND METHODS: RT-qPCR was conducted to detect CASC2 expression level in 63 LAC tissues and 4 LAC cells. Besides, statistical methods were applied to analyze clinical data and prognosis in the 63 patients. Furthermore, function experiments were performed to determine the effect of CASC2 on LAC metastasis in vitro. The potential mechanism was further explored by RT-qPCR and Western blot assay. RESULTS: In our study, CASC2 expression level was lower in LAC tissues than that in corresponding tissues. CASC2 expression was associated with lymph node metastasis, clinical stage and survival time of these patients. Moreover, overexpression of CASC2 inhibited migrated and invaded ability of LAC cells. Then, epithelial to mesenchymal transition (EMT) process of LAC cells and SOX4 expression was suppressed by upregulating CASC2. CONCLUSIONS: These results indicate that CASC2 could inhibit metastasis and EMT of LAC via suppressing SOX4, which may offer a new vision for interpreting the mechanism of LAC metastasis.