Long noncoding RNA UFC1 promotes metastasis and invasion of hepatocellular carcinoma cells via GSK-3β/β-catenin axis / 南方医科大学学报

OBJECTIVE@#To explore the role of Long noncoding RNA UFC1 (lincRNA-UFC1) in modulating the metastasis and invasion of hepatocellular carcinoma (HCC) cells and the underlying mechanism.@*METHODS@#Human HCC cell line Huh7 was infected with the lentiviral vector carrying lincRNA-UFC1 to obtain a cell line with lincRNA-UFC1 overexpression. A short hairpin RNA (shRNA) targeting lincRNA-UFC1 was delivered in human HCC BEL-7402 cells via a lentiviral vector to obtain a cell line with lincRNA-UFC1 knockdown. Expression levels of lincRNA-UFC1 in the two HCC cell lines were detected using real-time PCR, and the changes in the cell invasion and migration in response to lincRNA-UFC1 overexpression or knockdown were analyzed using Transwell and wound-healing assays. The expressions of GSK-3β/β-catenin-related proteins in the cells were detected with Western blotting. XAV-939, a GSK-3β/β-catenin inhibitor, was used for assessing the impact of lincRNAUFC1 overexpression on the invasion and migration of the HCC cells through Transwell and wound-healing assays.@*RESULTS@#Overexpression of lincRNA-UFC1 significantly promoted the invasion and migration of Huh7 cells as compared with the control cells ( < 0.001), while lincRNA-UFC1 knockdown obviously suppressed the invasion and migration of BEL-7402 cells ( < 0.001). The results of Western blotting showed that the expressions of proteins associated with the cell invasion and migration, namely β-catenin and P-GSK-3β, were significantly upregulated in response to lincRNA-UFC1 overexpression, and were obviously lowered after lincRNA-UFC1 knockdown. Treatment of the cells with XAV-939 significantly reversed the effect of lincRNA-UFC1 overexpression on the cell invasion and migration ( < 0.001).@*CONCLUSIONS@#lincRNA-UFC1 overexpresison promotes cell invasion and migration through the GSK-3β/β-catenin axis in HCC cells .

miR-128a is up-regulated in hepatocellular carcinoma and promotes tumor cell proliferation by targeting RND3 / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the expression of microRNA-128a (miR-128a) and its role in hepatocellular carcinoma (HCC).</p><p><b>METHODS</b>Nineteen pairs of fresh surgical specimens of HCC and adjacent tissues were examined for miR-128a expression using qRT-PCR. A miR-128a mimics or inhibitor was transfected into HCC cells, and the cell viability was analyzed by MTT assay. RND3, one of the potential targets of miR-128a, was predicted by bioinformatics software and demonstrated by dual luciferase reporter assay. The expression of RND3 after transfection was detected using qRT-PCR and Western blotting, and the cell cycle-related proteins were determined with Western blotting.</p><p><b>RESULTS</b>The expression of miR-128a were significantly up-regulated in HCC tissues as compared to the adjacent tissues (P<0.05). In cultured HCC cells, miR-128a promoted the cell proliferation and resulted in down-regulated RND3 mRNA and protein expressions by targeting RND3' 3'UTR (P<0.05) and also in the down-regulation of cyclin B1, cyclin D1 and CDK4 protein expressions.</p><p><b>CONCLUSION</b>miR-128a is up-regulated in HCC and promotes HCC cell proliferation by targeting RND3.</p>

Effect of casein kinase 2β in esophageal carcinoma and its clinical significance / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the expression of casein kinase 2β in esophageal carcinoma tissues and analyze its clinical significance.</p><p><b>METHODS</b>The expression of CK2β in a tissue chip containing 60 normal esophageal mucosa and 60 colorectal cancer specimens were detected immunohistochemically. Ten human esophageal carcinoma and adjacent normal tissues were examined for the expression of CK2β protein and mRNA using Western blotting and real-time quantitative PCR, respectively.</p><p><b>RESULTS</b>A strong expression of CK2β was found in 85.71% of the esophageal cancer tissues; 1.79% of the cancer tissues were negative for CK2β expression, and 1.79% and 10.71% of the cancer tissues were weakly and moderately positive, respectively. In the normal mucosal tissues, 96.67% of the tissues were negative for CK2β and 3.33% showed weak CK2β expression, showing a significant difference in the distribution of CK2β between normal and esophageal carcinoma tissues (P<0.001). The expression level of CK2β in esophageal cancers was associated with the pathological stage (TNM) (P=0.010). Western blotting and real-time quantitative PCR also confirmed an increased CK2β expression in the esophageal cancer tissues.</p><p><b>CONCLUSION</b>The high expression of protein kinase CK2β is closely related to the carcinogenesis and malignancy of esophageal cancer.</p>