miR-373 Inhibits Glioma Cell U251 Migration and Invasion by Down-Regulating CD44 and TGFBR2

Wei, Furong; Wang, Qianrong; Su, Qinghong; Huang, Haiyan; Luan, Junwen; Xu, Xiaoqun; Wang, Junfu

doi:10.1007/s10571-016-0338-3

Cited by 30 publications

(19 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As TGFb signaling is known to induce transcriptions factors ZEB1, ZEB2, and SNAI2, miR-520f might downregulate these transcription factors through targeting TGFBR2 (36,37). Furthermore, knockdown of TGFBR2 has been shown to inhibit tumor cell invasion (38,39). This is in line with our results showing that siRNA mediated knockdown of TGFBR2 inhibits tumor cell invasion.…”

Section: Discussionsupporting

confidence: 89%

miRNA-520f Reverses Epithelial-to-Mesenchymal Transition by TargetingADAM9andTGFBR2

et al. 2017

View full text Add to dashboard Cite

Reversing epithelial-to-mesenchymal transition (EMT) in cancer cells has been widely considered as an approach to combat cancer progression and therapeutic resistance, but a limited number of broadly comprehensive investigations of miRNAs involved in this process have been conducted. In this study, we screened a library of 1120 miRNA for their ability to transcriptionally activate the E-cadherin gene in a promoter reporter assay as a measure of EMT reversal. By this approach, we defined miR-520f as a novel EMT-reversing miRNA. miR-520f expression was sufficient to restore endogenous levels of E-cadherin in cancer cell lines exhibiting strong or intermediate mesenchymal phenotypes. In parallel, miR-520f inhibited invasive behavior in multiple cancer cell systems and reduced metastasis in an experimental mouse model of lung metastasis. Mechanistically, miR-520f inhibited tumor cell invasion by directly targeting, the TGFβ receptor and the EMT inducers, and the snail transcriptional repressor , each crucial factors in mediating EMT. Collectively, our results show that miR-520f exerts anti-invasive and antimetastatic effects and , warranting further study in clinical settings..

show abstract

Section: Discussionsupporting

confidence: 89%

miRNA-520f Reverses Epithelial-to-Mesenchymal Transition by TargetingADAM9andTGFBR2

et al. 2017

View full text Add to dashboard Cite

show abstract

“…Notably, the TGF-β-SMAD pathway confers poor prognosis to glioma patients and promotes cell proliferation (24). TGFBRII is a critical component of the TGF-β signaling pathway and TGFBRII silencing blocked the effects of TGF-β1 in glioma cells (25). In the present study, we found that miR-520c negatively regulated the abundance of TGFBRII in glioma cells.…”

Section: Discussionsupporting

confidence: 56%

MicroRNA-520c inhibits glioma cell migration and invasion by the suppression of transforming growth factor-β receptor type 2

Chen

Zhang

et al. 2017

Oncology Reports

View full text Add to dashboard Cite

Dysregulation of microRNAs (miRNAs) is actively involved in the development and progression of glioma. miR-520c was previously found to inhibit glioblastoma cell migration. However, the clinical significance of miR-520c and its biological function in glioma remain largely unknown. In the present study, we found that miR-520c expression in glioma tissues was significantly decreased compared to adjacent non‑cancerous tissues. The low level of miR-520c was prominently correlated with advanced World Health Organization (WHO) grade and decreased overall survival of glioma patients. Overexpression of miR-520c in U251 cells significantly decreased the migration and invasion of the cancer cells, while miR-520c silencing promoted U87 cell migration and invasion in vitro. Mechanistically, miR-520c inversely regulated transforming growth factor-β receptor type 2 (TGFBRII) abundance in the glioma cells. Herein, TGFBRII was found to be a downstream target of miR-520c in glioma. Furthermore, an inverse correlation between TGFBRII and miR-520c expression was observed in the glioma cases. In constrast, restoration of TGFBRII expression abrogated the effects of miR-520c overexpression in U251 cells with increased cell migration and invasion. In addition, miR-520c overexpression blocked TGF-β1‑induced cell migration and invasion in U251 cells. Collectively, miR-520c may serve as a prognostic predictor and a therapeutic target for glioma patients.

show abstract

“…Consistent with this evidence, the results in this study showed that the ectopic expression of miR-373 reduced VM formation in U87 and U251 glioma cells. Wei et al [54] showed that miR-373 inhibits U251 glioma cell migration and invasion but does not affect proliferation in U251 cells. However, our results showed that miR-373 suppressed malignant behaviors inU87 and U251 cells, including cell viability.…”

Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNA HOXA-AS2 Regulates Malignant Glioma Behaviors and Vasculogenic Mimicry Formation via the MiR-373/EGFR Axis

Gao

Liu

et al. 2017

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Vasculogenic mimicry (VM) has been reported to be a novel glioma neovascularization process. Anti-VM therapy provides new insight into glioma clinical management. In this study, we revealed the role of the long non-coding RNA HOXA cluster antisense RNA 2 (HOXA-AS2) in malignant glioma behaviors and VM formation. Methods: Quantitative real-time PCR was performed to determine the expression levels of HOXA-AS2 in glioma samples and glioblastoma cell lines. CD34-periodic acid-Schiff dual-staining was performed to assess VM in glioma samples. CCK-8, transwell, and Matrigel tube formation assays were performed to measure the effects of HOXA-AS2 knockdown on cell viability, migration, invasion, and VM tube formation, respectively. RNA immunoprecipitation, dual-luciferase reporter and Western blot assays were performed to explore the molecular mechanisms underlying the functions of HOXS-AS2 in glioblastoma cells. A nude mouse xenograft model was used to investigate the role of HOXA-AS2 in xenograft glioma growth and VM density. Student’s t-tests, one-way ANOVAs followed by Bonferroni posthoc tests, and chi-square tests were used for the statistical analyses. Results: HOXA-AS2 was upregulated in glioma samples and cell lines and was positively correlated with VM. HOXA-AS2 knockdown attenuated cell viability, migration, invasion, and VM formation in glioma cells and inhibited the expression of vascular endothelial-cadherin (VE-cadherin), as well as the expression and activity of matrix metalloproteinase matrix metalloproteinase (MMP)-2 and MMP-9. miR-373 was downregulated in glioma samples and cell lines and suppressed malignancy in glioblastoma cells. HOXA-AS2 bound to miR-373 and negatively regulated its expression. Epidermal growth factor receptor (EGFR), a target of miR-373, increased the expression levels of VE-cadherin, as well as the expression and activity levels of MMP-2 and MMP-9, via activating phosphatidylinositol 3-kinase/serine/threonine kinase pathways. HOXA-AS2 knockdown combined with miR-373 overexpression yielded optimal tumor suppressive effects and the lowest VM density in vivo. Conclusion: HOXA-AS2 knockdown inhibited malignant glioma behaviors and VM formation via the miR-373/EGFR axis.

show abstract

miR-373 Inhibits Glioma Cell U251 Migration and Invasion by Down-Regulating CD44 and TGFBR2

Cited by 30 publications

References 43 publications

miRNA-520f Reverses Epithelial-to-Mesenchymal Transition by TargetingADAM9andTGFBR2

miRNA-520f Reverses Epithelial-to-Mesenchymal Transition by TargetingADAM9andTGFBR2

MicroRNA-520c inhibits glioma cell migration and invasion by the suppression of transforming growth factor-β receptor type 2

Long Non-Coding RNA HOXA-AS2 Regulates Malignant Glioma Behaviors and Vasculogenic Mimicry Formation via the MiR-373/EGFR Axis

Contact Info

Product

Resources

About