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Introduction: Previous studies have shown that the dysregulation of miRNAs are frequently associated with cancer progression. Deregulation of miR-211 has been observed in various types of human cancers. However, its biological function in gastric cancer (GC) is still unknown., Methods: The expression of miR-211 in GC was detected by using quantitative real-time PCR (qRT-PCR). The miR-211 mimics and inhibitor were designed and transfected into BGC-823 cells. Then, we explore the probable biological function of miR-211 in gastric cancer cell proliferation and invasion in vitro. A luciferase reporter assay and western blot were performed to confirm the target gene of miR-211., Results: MiR-211 was significantly down-regulated in GC. Over-expression of miR-211 inhibited gastric cancer cell proliferation and invasion in vitro, conversely, down-regulated expression of miR-211 promoted gastric cancer cell proliferation and invasion. In addition, the sex-determining region Y-related high mobility group box 4 (SOX4) is identified as a target of miR-211 in GC cells, and SOX4 expression levels was inversely correlated with miR-211. Furthermore, knockdown of Sox4 inhibited the proliferation and invasion in GC cells., Conclusion: miR-211 could inhibit GC cell proliferation and invasion partially by down-regulating SOX4. MiR-211 might be a potential therapeutic target for GC treatment in the future.

Background: MicroRNAs (miRNA) have been documented playing a critical role in cancer progression. Although miR-338-3p has been implicated in several cancers, its role in gastric cancer is still unknown. The aim of our study was to investigate the role of miR-338-3p in gastric cancer progression., Methods: Expression levels of miR-338-3p in gastric cancer cell lines and tissues were determined by quantitative real-time PCR (qRT-PCR). The effect of miR-338-3p on proliferation was evaluated by MTT assay, cell migration and invasion were evaluated by transwell migration and invasion assays. Furthermore, luciferase reporter assay was conducted to confirm the target gene of miR-338-3p, and the results were validated in gastric cancer cells., Results: In the present study, we found that miR-338-3p was down-regulated in both gastric cancer cell lines and tissues. Enforced expression of miR-338-3p inhibited proliferation, migration and invasion of gastric cancer cells in vitro. Moreover, we identified A disintegrin and metalloproteinase 17 (ADAM17) gene as potential target of miR-338-3p. Importantly, ADAM17 rescued the miR-338-3p mediated inhibition of cell proliferation, migration and invasion., Conclusions: Our study suggested that miR-338-3p is significantly decreased in gastric cancer, and inhibits cell proliferation, migration and invasion partially via the downregulation of ADAM17. Thus, miR-338-3p may represent a potential therapeutic target for gastric cancer intervention.

Background: A large number of studies demonstrated that microRNAs play important roles in the progression and development of human cancers. However, the expression level of miR-107 and its biological function in hepatocellular carcinoma (HCC) remains unclear., Method: Quantitative real-time PCR (qRT-PCR) was used to evaluate the expression level of miR-107 in HCC tissues and cell lines. Then, we explored the function of miR-107 to determine its potential roles on HCC cell proliferation in vitro. Luciferase reporter assay was used to confirm the target gene of miR-107, and the results were validated in cell lines., Results: miR-107 was significantly up-regulated in HCC tissues and cell lines. The enforced expression of miR-107 was able to promote cell proliferation in HepG2 cells. At the molecular level, our results suggested that expression of Axin2 was negatively regulated by miR-107., Conclusion: Our observations suggested that miR-107 could promote HCC cells proliferation via targeting Axin2 and might represent a potential therapeutic target for HCC.

Introduction: long non-coding RNA ANRIL (lncRNA ANRIL) has been demonstrated to play a crucial role in cancer progression. However, its effects in hepatocellular carcinoma (HCC) have not been explored. The aim of this study was to investigate the clinical significance of lncRNA NRIL in human HCC., Methods: In this study, we determined for the first time the expression of lncRNA ANRIL in human HCC by quantitative Real-time-PCR analysis. Kaplan-Meier curves and multivariate Cox proportional models were used to study the impact on clinical outcome. Small interfering RNA (siRNA) was used to silence lncRNA ANRIL and to explore the effects of reduced lncRNA ANRIL expression on cell growth and metastasis., Results: lncRNA ANRIL expression in HCC tissues was significantly higher than in the adjacent non-tumor tissues (P<0.05). The expression of lncRNA ANRIL was remarkably associated with the histologic grade and TNM stage of HCC patients (P<0.05). In addition, HCC patients with higher lncRNA ANRIL expression had significantly poorer overall survival (P<0.05). Multivariate analysis suggested that high lncRNA ANRIL expression was an independent predictor of poor prognosis (P<0.05). Moreover, in vitro assays revealed that the decreased expression of lncRNA ANRIL could suppress the cell proliferation, migration and invasion HCC cells., Conclusions: Our results suggest that lncRNA ANRIL may serve as an efficient clinical biomarker and a therapeutic target for HCC patients.

Introduction: Dysregulation of long non-coding RNAs (lncRNAs) play important roles in tumor progression. The aim of our study was to explore the clinicopathologic and prognostic significance of lncRNA CCAT2 expression in human gastric cancer., Methods: Expression levels of lncRNA CCAT2 in 85 pairs of gastric cancer and adjacent non-tumor tissues were detected by quantitative real-time PCR (qRT-PCR). In order to determine its prognostic value, overall survival and progression-free survival were evaluated using the Kaplan-Meier method, and multivariate analysis was performed using the Cox proportional hazard analysis., Results: Expression levels of lncRNA CCAT2 in gastric cancer tissues were significantly higher than those in adjacent non-tumor tissues. By statistical analyses, high lncRNA CCAT2 expression was observed to be closely correlated with higher incidence of lymph node metastasis and distance metastasis. Moreover, patients with high lncRNA CCAT2 expression had shorter overall survival and progression-free survival compared with the low lncRNA CCAT2 group. Multivariate analyses indicated that high lncRNA CCAT2 expression was an independent poor prognostic factor for gastric cancer patients., Conclusions: Our results suggested that up-regulation of lncRNA CCAT2 was correlated with gastric cancer progression, and lncRNA CCAT2 might be a potential molecular biomarker for predicting the prognosis of patients.

Objective: To induce the differentiation of human bone marrow mesenchymal stem cells (HMSCs) into hepatocyte-like cells with hepatocyte growth factor (HGF) and fibroblast growth factor-4 (FGF-4) in vitro., Methods: HMSCs were induced to differentiate into hepatocyte-like cells by HGF (group B), FGF-4 (group C) and HGF+FGF-4 (group D) in vitro. Undifferentiated HMSCs and L-02 cells were used as the negative (group A) and positive (group E) controls, respectively. The changes of cell morphology were observed microscopically. The expressions of hepatic markers, alpha fetoprotein (AFP) and CK-18, were detected by immunocytochemical staining at different times after induction, and the differentiation ratios of the various groups of HMSCs were calculated on the basis of image analysis. The expressions of AFP and ALB were detected by immunofluorescence assay in each group at different times after induction, and the expressions of AFP and ALB mRNA by RT-PCR., Results: HMSCs gradually transformed into spindle-shaped, round, polygonal or irregular cells after induction. Immunocytochemical staining revealed positive AFP and CK18 expressions in groups B, C, and D after induction as well as in group E. The positive units (PU) of AFP and CK18 in group D calculated according to image analysis were significantly higher than that of groups A, B, and C. The expressions of AFP and ALB detected by immunofluorescence were both positive after induction in all groups except group A, similar to the findings of the expressions of AFP and ALB mRNA by RT-PCR., Conclusion: HMSCs can be induced to differentiate into hepatocyte-like cells by HGF, FGF-4 and their combination at certain concentrations, and the hepatocyte-like cells can express some hepatic markers such as AFP, ALB, CK18, etc. HGF+FGF-4 may achieve more effective induction of HMSC differentiation into hepatocyte-like cells, and the efficiency of HGF is greater than that of FGF-4.