ABSTRACT
@#[Abstract] Objective: To investigate the expression of lncRNA linc01503 in esophageal squamous cell carcinoma (ESCC) tissues and cell lines, as well as its effect on the proliferation, invasion and epithelial-mesenchymal transition (EMT) of ESCC cells. Methods: A total of 119 pairs of tumor tissues and corresponding para-cancerous tissues of ESCC patients were obtained from the Fourth Affiliated Hospital of Hebei Medical University between Jan. 2012 and Dec. 2014. The expression of linc01503 in ESCC tissues and cell lines (Kyse150, Kyse170, Eca109, TE1 and TE13) was detected by qPCR. The ESCC cells were transfected with pGPU6-shRNA-linc01503 or treated with TGF-β. The expressions of EMT related genes before and after transfection as well as linc01503 expression before and after TGF-β treatment were detected with qPCR. MTS and Transwell assay were performed to assess the effect of linc01503 on proliferation and invasion of ESCC cells. Results: The expression of linc01503 was significantly elevated in ESCC tissues and cell lines (all P<0.05). High expression of linc01503 was correlated with lymph node metastasis, depth of infiltration, TNM stage and the survival of ESCC patients (all P<0.05). Treatment with TGF-β promoted EMT of ESCC cells and induced a significant up-regulation of linc01503 expression. Knockdown of linc01503 significantly inhibited proliferation and invasion ability of ESCC cells; Meanwhile, the low expression of linc01503 increased the expression of E-cadherin but decreased the expressions of N-cadherin and vimentin (all P<0.05). Conclusion: lncRNA linc01503, as one of the downstream effect genes of TGF- β, promotes the proliferation, invasion and EMT process of ESCC cells.
ABSTRACT
@#Objective: To screen the Hub genes associated with the occurrence and development of esophageal squamous cell carcinoma (ESCC) and to analyze their biological functions by using various bioinformatics analysis tools. Methods: ESCC chip profile GSE100942 from GEO database was used as study subject; GEO2R tool was used to analyze the data and to screen the differentially expressed genes (DEGs), and the bioinformatics tools (DAVID, String, Cytoscape) were further used to construct protein-protein interaction (PPI) network and identify the key Hub genes. GO and KEGG were used for the biological function enrichment analysis. In the meanwhile, MiRDB was applied to identify the miRNAs that might regulate Hub genes and to construct Hub gene–miRNA network. Importantly, the expression of DEGs and the patient survival were verified by the GEPIA analysis tool. Results: By analyzing GSE100942 database, a total of 1229 DEGs with difference of 2 times and 223 DEGs with difference of 4 times were screened out. In addition, 20 Hub genes, which were all up-regulated in ESCC tissues, were also identified. The functional enrichment analysis showed that these DEGs were mainly enriched in cancer related pathways and involved in cell division and mitotic nuclear division. Among those 20 Hub genes, DLGAP5, BUB1B, TPX2, TTK, CDC20, CCNB2, AURKA and DEPDC1 were identified as 8 key Hub genes that related with ESCC, and involved in many important biological processes, such as cell proliferation, cell cycle and signal pathway. Five Hub genes, CEP55, ECT2, NEK2, DEPDC1 and NUSAP1, were identified to be highly regulated by the miRNA regulatory network. Conclusion: Microarray combined with bioinformatics can effectively analyze the DEGs associated with the occurrence and development of ESCC. The identification of the 20 Hub genes and the 8 key Hub genes can provide theoretical guidance for further research on the molecular mechanism and molecular marker screening of ESCC. ·