H19 Functions as a Competing Endogenous RNA to Regulate EMT by Sponging miR-130a-3p in Glioma

Hu, Qi; Yin, Jianxing; Zeng, Ailiang; Jin, Xin; Zhang, Zhuoran; Yan, Wei; You, Yongping

doi:10.1159/000494002

Cited by 59 publications

(36 citation statements)

References 35 publications

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“…These findings are in agreement with the promoting role of RIOK2 and the inhibitory effects of miR‐4744 in the migration and invasion of glioma cell. It should be noted that we failed to show the changes of E‐cadherin, probably due to its low expression in glioma cell lines as reported previously 32 . In addition, the mechanism by which RIOK2/miR‐4744 regulates the EMT process deserves further studies in glioma cells.…”

Section: Discussionmentioning

confidence: 42%

RIOK2 is negatively regulated by miR‐4744 and promotes glioma cell migration/invasion through epithelial‐mesenchymal transition

Song

Cheng

Jin

et al. 2020

J Cellular Molecular Medi

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RIOK2 is a member of RIO (right open reading frame) kinase family. Recent studies have revealed the involvement of RIO kinases in glioma cell growth and expansion. However, the role and mechanism of RIOK2 in glioma cell migration and invasion remain unclear. Wound healing assay, Transwell assay and real-time quantitative PCR (qRT-PCR) detection of matrix metalloproteinases (MMPs) were used to evaluate the migration/invasion of glioma cells. Western blot and qRT-PCR were employed to measure the expression of epithelial-mesenchymal transition (EMT) markers. Dual luciferase reporter assay was performed to determine the binding between RIOK2 and miR-4744. In addition, RIOK2 and miR-4744 levels were quantified by qRT-PCR and/ or immunohistochemistry in glioma tissues. Transfection of RIOK2 siRNAs significantly inhibited glioma cell migration and invasion and down-regulated the expression of MMPs (MMP2 and MMP9) and mesenchymal markers (N-cadherin, β-catenin, Twist1, fibronectin, ZEB-1) in glioma cells. Overexpression of RIOK2 showed the opposite effects. MiR-4744 directly bound to the 3'-untranslated region of RIOK2 and negatively regulated the expression of RIOK2. Up-regulation of miR-4744 inhibited the migration and invasion of glioma cells. Overexpression of RIOK2 could reverse the effects of miR-4744 up-regulation on the migration, invasion and EMT process in glioma cells. Moreover, RIOK2 was high, while miR-4744 was low in glioma tissues, and a negative correlation was found between them. These results suggest that RIOK2 is post-transcriptionally targeted by miR-4744, the low miR-4744 and high RIOK2 levels in glioma may contribute to tumour cell infiltration through promoting the EMT. K E Y W O R D S fibronectin, glioma, miR-4744, N-cadherin, RIOK2, β-catenin | 4495 SONG et al. S U PP O RTI N G I N FO R M ATI O N Additional supporting information may be found online in the Supporting Information section. How to cite this article: Song Y, Li C, Jin L, et al. RIOK2 is negatively regulated by miR-4744 and promotes glioma cell migration/invasion through epithelial-mesenchymal transition.

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Section: Discussionmentioning

confidence: 42%

RIOK2 is negatively regulated by miR‐4744 and promotes glioma cell migration/invasion through epithelial‐mesenchymal transition

Song

Cheng

Jin

et al. 2020

J Cellular Molecular Medi

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“…CeRNA is a known mechanism of lncRNA; in this mechanism, lncRNA competes for posttranscriptional control by sponging certain relevant miRNAs . Previous surveys have confirmed some lncRNA‐miRNA interaction pathways, which provide some theoretical basis for our current research.…”

Section: Introductionmentioning

confidence: 76%

Long noncoding RNA ENST00000413528 sponges microRNA‐593‐5p to modulate human glioma growth via polo‐like kinase 1

Zhang

Wei

et al. 2019

CNS Neurosci Ther

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Summary Aims In this study, we examined the expression of lncRNA ENST00000413528 in glioma and determined its role in glioma development. Methods LncRNA ENST00000413528 was detected in glioma tissues by lncRNA microarray. Then, we performed real‐time PCR, CCK‐8, colony formation assay, flow cytometry, caspase‐3/7 assay and animal experiment to detect the function of ENST00000413528 in glioma after ENST00000413528 knockdown. Subsequent bioinformatics analysis, luciferase reporter assays and RNA immunoprecipitation (RIP) assay western blotting indicated possible downstream regulatory molecules. The expression of PLK1 in glioma tissues was also examined by immunohistochemistry staining. Results Expression of ENST00000413528 was significantly increased in glioma tissues and LN229 and U251 cells. PLK1 protein could not be detected in peritumoral brain edema (PTBE) tissues; however, it showed an increasing number of positively cytoplasmic stained from WHO‐Grade II to Grade III gliomas. Knockdown of ENST00000413528 in glioma cells inhibited cell proliferation and colony formation abilities, induced the G0/G1 arrest of the cell cycle, and promoted apoptosis. The dual reporter assay and RNA immunoprecipitation assay verified the interaction between ENST00000413528 and miR‐593. We also demonstrated that polo‐like kinase 1 (PLK1) was regulated by miR‐593; PLK1 messenger RNA lacking 3’UTR partially reversed the effects caused by ENST00000413528 knockdown or miR‐593 upregulation. Conclusion lncRNA ENST00000413528 is closely related to the development of glioma via the miR‐593‐5p/PLK1 pathway.

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“…These findings suggest that syncytin-1 may be a regulatory gene for EC. EMT is an effective way for epithelial cells to acquire migratory capacity [41][42][43][44][45][46][47][48] and has become an important pathway for invasion and metastasis of epithelial cell carcinoma. Various studies showed that the development of EMT is accompanied with changes in markers, including E-cadherin, N-cadherin, and vimentin.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of syncytin-1 promotes invasion and metastasis by activating epithelial-mesenchymal transition-related pathway in endometrial carcinoma

Liu

Wen

et al. 2018

OTT

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Background: Endometrial carcinoma (EC) is the most common and lethal malignancy worldwide. Syncytin-1 is expressed in multiple types of cancer. However, the expression pattern and potential mechanism of syncytin-1 and its clinical significance in EC remain unclear. Materials and methods: We analyzed 130 primary EC specimens from Binzhou Medical University to investigate the clinical role of syncytin-1 in EC by using different advanced pathological stages of EC tissues. Kaplan-Meier analysis was used to measure the overall survival of EC patients. Syncytin-1 expression was analyzed by Western blot assays in HECCL-1 and RL-95-2 cells. Cell proliferation, cycle, migration, and invasion abilities were detected by cell counting kit-8, flow cytometry, and transwell assays. AKT and epithelial-mesenchymal transition (EMT)-related genes were assessed by Western blot assays in HECCL-1 and RL-95-2 cells. Results: Syncytin-1 was upregulated in EC tissues and cells and was related to clinical stages, expression of ER, Ki-67, and overall survival of EC. Functional research revealed that overexpression of syncytin-1 can promote cell proliferation, cell cycle progression, and the migration and invasion of EC cells. Suppression of syncytin-1 expression also inhibited cell proliferation and apoptosis in vitro. The expression of syncytin-1 substantially improved the expression levels of EMT-related genes (vimentin, E-cadherin, slug, and ZEB1) but significantly decreased those of epithelial markers (N-cadherin and snail). In addition, we found that syncytin-1 was not correlated with AKT-related genes (total-AKT, p-AKT, and vinculin). Conclusion: Our results suggested that syncytin-1 may promote aggressive behavior and can serve as a novel prognostic biomarker for EC. Our study provides new insights into the regulatory mechanism of EMT signaling.

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H19 Functions as a Competing Endogenous RNA to Regulate EMT by Sponging miR-130a-3p in Glioma

Cited by 59 publications

References 35 publications

RIOK2 is negatively regulated by miR‐4744 and promotes glioma cell migration/invasion through epithelial‐mesenchymal transition

RIOK2 is negatively regulated by miR‐4744 and promotes glioma cell migration/invasion through epithelial‐mesenchymal transition

Long noncoding RNA ENST00000413528 sponges microRNA‐593‐5p to modulate human glioma growth via polo‐like kinase 1

Upregulation of syncytin-1 promotes invasion and metastasis by activating epithelial-mesenchymal transition-related pathway in endometrial carcinoma

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