OBJECTIVE: This study aimed to investigate the role of long non-coding RNA MEG3 (lncRNA MEG3) in osteosarcoma (OS) and further explore the underlying molecular mechanism. MATERIALS AND METHODS: The expression profi les of MEG3 in OS cell lines and normal osteoblast cell line were detected by qRT-PCR. MEG3 was over-expressed in OS cell line by using LV-MEG3. MTT and colonyformation assays were applied for cell proliferation analysis. Cell migration assay was applied to investigate the cell migration ability. In addition, the expression levels of cell growth and metastasis related factors (Notch1, Hes1, TGF-β, N-cadheren and E-cadheren) were determined to illustrate the mechanisms. RESULTS: We found that compared with normal osteoblast hFOB1.19 cell line, MEG3 was signifi cantly downregulated in MG63 and U2OS cell lines, particularly in MG-63 cells. MEG3 was signifi cantly up-regulated in MG63 cells by LV-MEG3. Cell proliferation and migration ability were obviously repressed by MEG3 over-expression. In addition, MEG3 over-expression markedly inhibited Notch1, Hes1,TGF-β and N-cadheren expression, and the expression level of E-cadheren was improved. CONCLUSIONS: These results indicated that MEG3 could prevent cell growth and metastasis of OS by repressing Notch and TGF-β signaling pathway, thus providing a potential therapeutic target for OS treatment (Tab. 1, Fig. 4, Ref. 30). Text in PDF www.elis.sk.

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Despite the poor prognosis of oesophageal cancer (EC), the molecular mechanisms of EC are still unclear. In recent years, role of lncRNA in cancer development attracted much attention. The present study aimed to investigate the effects of the long noncoding RNA SNHG1 on the migration and invasion of EC cells and the possible mechanisms involved. The effects of SNHG1 on cell proliferation, migration, and invasion were determined and its relationship with miR‐195/Cdc42 axis was investigated. It was found SNHG1 and Cdc42 were significantly upregulated, and miR‐195 was significantly downregulated in both EC tissues and cell lines. In addition, the inhibition of either SNHG1 or Cdc42 resulted in suppression of cell proliferation, migration, and invasion, while inhibition of miR‐195 led to opposite results and reversed the effects of si‐SNHG1. We also observed that higher SNHG1 predicted poorer prognosis of EC patients. In summary, inhibition of SNHG1 can suppress the cell migration and invasion of EC cells by sponging miR‐195 through targeting Cdc42. This study might provide deeper insights into the SNHG1/miR‐195/Cdc42 axis in EC.

Aim MiR‐326 has been investigated to be correlated with multiple types of malignancies; however, the role of miR‐326 in endometrial cancer (EC) remains rarely reported. The aim of our research is to investigate the functions of miR‐326 in EC and the potential molecular mechanism. Methods RT‐qPCR was performed to compare the expression of miR‐326 and Bcl‐2 in normal endometrial epithelial cell line (End1/e6e7) and EC cells lines (HEC‐1A, Ishikawa), respectively. Bioinformatic analysis and luciferase assay verified the relationship between miR‐326 and the 3’‐UTR of Bcl‐2. 3‐(4,5‐dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2‐H‐tetrazolium bromide (MTT) assay, soft agar colony formation assay and the flow cytometry were performed to investigate the functions of miR‐326 and Bcl‐2 on proliferation and apoptosis in EC. Western blotting was employed to explore the expression of Bcl‐2, Bcl2‐associated X (Bax) and caspase‐3. Results The expression of miR‐326 decreased in EC cell lines compared to normal endometrial epithelial cell line, while Bcl‐2 expression was increased in EC cells. Results of MTT and soft agar colony formation assays showed that miR‐326 suppressed proliferation in EC cells. In addition, flow cytometry revealed that miR‐326 promoted apoptosis in EC cells. Western blotting showed that silencing miR‐326 promoted the expression of Bcl‐2. Bioinformatics analysis and luciferase assay verified the 3’‐UTR of Bcl‐2 was a target of miR‐326. Furthermore, MTT assay, soft agar colony formation assay and the flow cytometry proved that miR‐326 acts as tumor suppressor via inhibiting the expression of Bcl‐2. Conclusion MiR‐326 acts as a cancer suppressor to inhibit proliferation and promote apoptosis via targeting Bcl‐2 axis in EC.