scholarly journals Long non-coding RNA SNHG6 promotes glioma tumorigenesis by sponging miR-101-3p

2018 ◽  
Vol 33 (2) ◽  
pp. 148-155 ◽  
Author(s):  
Qiang Meng ◽  
Bao-Ying Yang ◽  
Bei Liu ◽  
Ji-Xue Yang ◽  
Yang Sun
Keyword(s):  
Cell Proliferation ◽  
Poor Prognosis ◽  
Epithelial Mesenchymal Transition ◽  
Primary Brain Tumor ◽  
Normal Brain ◽  
Mesenchymal Transition ◽  
Non Coding Rna ◽  
Tumor Tissues ◽  
Glioma Cell Proliferation ◽  
Long Non Coding Rna

Introduction: Glioma is the most common primary brain tumor. The small nucleolar RNA host gene (SNHG) SNHG6 is a potential oncogene in the development of several types of cancers. Methods: In this study, we investigated the functional role of long non-coding RNA (lncRNA) SNHG6 in the malignancy of glioma in cell lines and transplanted nude mice. Results: We found that the expression of lncRNA SNHG6 was higher in glioma tissues and cells than in normal brain tissues and cells. The expression of lncRNA SNHG6 was positively correlated with the malignancy and poor prognosis of glioma patients. microRNA (miR)-101-3p expression was decreased in glioma tissues and cells and was negatively correlated with the malignancy and poor prognosis of glioma patients. In glioma tissues, the expression of lncRNA SNHG6 was negatively correlated with the expression of miR-101-3p. SNHG6 contained a binding site of miR-101-3p. Knockdown of SNHG6 expression resulted in a significant increase of miR-101-3p expression. miR-101-3p mimic markedly decreased the luciferase activity of SNHG6. Knockdown of SNHG6 inhibited glioma cell proliferation, migration, and epithelial-mesenchymal transition (EMT), and increased apoptosis. miR-101-3p mimic enhanced knockdown of SNHG6-induced inhibition of cell proliferation, migration, and EMT, and an increase of apoptosis. Anti-miR-101-3p reversed the the effects of si-SNHG6 on cell malignancy. Knockdown of SNHG6 remarkably reduced the increase of tumor volumes in xenograft mouse models. In tumor tissues, knockdown of SNHG6 increased the expression of miR-101-3p and reduced EMT biomarker expression. Conclusions: Our study provides novel insights into the functions of lncRNA SNHG6/miR-101-3p axis in the tumorigenesis of glioma.

scholarly journals Long non-coding RNA FOXD2-AS1 promotes cell proliferation, metastasis and EMT in glioma by sponging miR-506-5p

Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 921-931
Author(s):  
Juan Zhao ◽  
Xue-Bin Zeng ◽  
Hong-Yan Zhang ◽  
Jie-Wei Xiang ◽  
Yu-Song Liu
Keyword(s):  
Cell Proliferation ◽  
Epithelial Mesenchymal Transition ◽  
Human Cancer ◽  
Glioma Cells ◽  
Suppressor Gene ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Non Coding Rna ◽  
Long Non Coding Rna

AbstractLong non-coding RNA forkhead box D2 adjacent opposite strand RNA 1 (FOXD2-AS1) has emerged as a potential oncogene in several tumors. However, its biological function and potential regulatory mechanism in glioma have not been fully investigated to date. In the present study, RT-qPCR was conducted to detect the levels of FOXD2-AS1 and microRNA (miR)-506-5p, and western blot assays were performed to measure the expression of CDK2, cyclinE1, P21, matrix metalloproteinase (MMP)7, MMP9, N-cadherin, E-cadherin and vimentin in glioma cells. A luciferase reporter assay was performed to verify the direct targeting of miR-506-5p by FOXD2-AS1. Subsequently, cell viability was analyzed using the CCK-8 assay. Cell migration and invasion were analyzed using Transwell and wound healing assays, respectively. The results demonstrated that FOXD2-AS1 was significantly overexpressed in glioma cells, particularly in U251 cells. Knockdown of FOXD2-AS1 in glioma cells significantly inhibited cell proliferation, migration, invasion and epithelial–mesenchymal transition (EMT) and regulated the expression of CDK2, cyclinE1, P21, MMP7 and MMP9. Next, a possible mechanism for these results was explored, and it was observed that FOXD2-AS1 binds to and negatively regulates miR-506-5p, which is known to be a tumor-suppressor gene in certain human cancer types. Furthermore, overexpression of miR-506-5p significantly inhibited cell proliferation, migration, invasion and EMT, and these effects could be reversed by transfecting FOXD2-AS1 into the cells. In conclusion, our data suggested that FOXD2-AS1 contributed to glioma proliferation, metastasis and EMT via competitively binding to miR-506-5p. FOXD2-AS1 may be a promising target for therapy in patients with glioma.

scholarly journals Long non-coding RNA MALAT1 regulated ATAD2 to facilitate retinoblastoma progression by sponging miR-655-3p

2020 ◽  
Author(s):  
Yuxin Zhao ◽  
Zhaoxia Wang ◽  
Meili Gao ◽  
Xuehong Wang ◽  
Hui Feng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Mesenchymal Transition ◽  
B Cell Lymphoma ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Western Blot Assay ◽  
Mesenchymal Transition ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Background: Long non-coding RNA (lncRNA) metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was reported as an oncogene in many tumors including retinoblastoma (RB). This research mainly focused on the functions and mechanism of MALAT1 in RB.Methods: The levels of MALAT1, microRNA-655-3p (miR-655-3p), and ATPase family AAA domain containing 2 (ATAD2) in RB tissues and cells were measured by quantitative real-time polymerase chain reaction (qRT-PCR). The cell viability and apoptotic rate were monitored via cell counting kit 8 (CCK8) assay and flow cytometry, respectively. The protein levels of p21, CyclinD1, B-cell lymphoma-2 (Bcl-2), cleaved-casp-3, E-cadherin, Ncadherin, Vimentin, and ATAD2 were detected by Western blot assay. Transwell assay was performed to estimate the abilities of migration and invasion. The interactions between miR-655-3p and MALAT1 or ATAD2 were predicted by starBase. Dual-luciferase reporter assay was constructed to verify these interactions. The mice model experiments were established to validate the effects of MALAT1 in vivo.Results: MALAT1and ATAD2 were significantly increased while the level of miR-655-3p was remarkably decreased in RB tissues and cells. MALAT1 knockdown inhibited cell proliferation, metastasis, and epithelial-mesenchymal transition (EMT) but promoted apoptosis via miR-655-3p in vitro, and blocked xenograft tumor growth in vivo. MALAT1 was validated to sponge miR-655-3p and ATAD2 was verified as a candidate of miR-655-3p. MiR-655-3p overexpression inhibited cell proliferation but promoted apoptosis by targeting ATAD2. MALAT1 silencing affected cell behaviors by regulating ATAD2. MALAT1 depletion down-regulated ATAD2 expression via miR-655-3p in RB cells.Conclusion: MALAT1 positively regulated ATAD2 to accelerate cell proliferation but retard apoptosis by sponging miR-655-3p in RB cells.

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