CircNT5E Acts as a Sponge of miR-422a to Promote Glioblastoma Tumorigenesis

Wang, Renjie; Zhang, Sai; Chen, Xuyi; Li, Nan; Li, Jianwei; Jia, Ruichao; Pan, Yuanqing; Liang, Haiqian

doi:10.1158/0008-5472.can-18-0532

Cited by 249 publications

(232 citation statements)

References 58 publications

(77 reference statements)

Supporting

Mentioning

221

Contrasting

Unclassified

Order By: Relevance

“…CircNT5E controls multiple pathologic processes, including cell proliferation, migration, and invasion, by directly sponging miR-422a and inhibiting its activity. Furthermore, circNT5E was observed to sponge other miRNAs, suggesting the existence of a more complex regulatory network controlled by circNT5E in GBM [122].…”

Section: Back Splicing In Brain Tumorsmentioning

confidence: 95%

Splicing Dysregulation as Oncogenic Driver and Passenger Factor in Brain Tumors

Bielli

Pagliarini

Pieraccioli

et al. 2019

Cells

View full text Add to dashboard Cite

Brain tumors are a heterogeneous group of neoplasms ranging from almost benign to highly aggressive phenotypes. The malignancy of these tumors mostly relies on gene expression reprogramming, which is frequently accompanied by the aberrant regulation of RNA processing mechanisms. In brain tumors, defects in alternative splicing result either from the dysregulation of expression and activity of splicing factors, or from mutations in the genes encoding splicing machinery components. Aberrant splicing regulation can generate dysfunctional proteins that lead to modification of fundamental physiological cellular processes, thus contributing to the development or progression of brain tumors. Herein, we summarize the current knowledge on splicing abnormalities in brain tumors and how these alterations contribute to the disease by sustaining proliferative signaling, escaping growth suppressors, or establishing a tumor microenvironment that fosters angiogenesis and intercellular communications. Lastly, we review recent efforts aimed at developing novel splicing-targeted cancer therapies, which employ oligonucleotide-based approaches or chemical modulators of alternative splicing that elicit an impact on brain tumor biology.

show abstract

Section: Back Splicing In Brain Tumorsmentioning

confidence: 95%

Splicing Dysregulation as Oncogenic Driver and Passenger Factor in Brain Tumors

Bielli

Pagliarini

Pieraccioli

et al. 2019

Cells

View full text Add to dashboard Cite

show abstract

“…18 For example, circ_0005230 was proved to be a dismal prognostic marker for breast cancer patients. 7 In this study, we found that upregulation of circ-CDC45 is related to larger tumor size and higher WHO grades. Recently, circ-CDC45 was identified enhanced in GM tissues than that in the normal tissues screened by circRNA microarray.…”

Section: Discussionmentioning

confidence: 54%

Overexpression of circular RNA circ‐CDC45 facilitates glioma cell progression by sponging miR‐516b and miR‐527 and predicts an adverse prognosis

Liu

Hou

et al. 2019

J of Cellular Biochemistry

View full text Add to dashboard Cite

Glioma (GM) is a highly lethal human cancer. Circular RNAs (circRNAs) act as an imperative factor in oncogenesis. We aimed to investigate the biological functions and mechanisms of circ‐CDC45 in GM. circ‐CDC45 expression in GM specimens and cell lines was measured by real‐time quantitative reverse transcription polymerase chain reaction. Fisher's exact test and Kaplan‐Meier curves further analyzed its clinical implications. A gain/loss‐of‐function study was conducted to investigate the role of circ‐CDC45 in GM. Additionally, luciferase reporter and rescue assays were performed to unravel the mechanisms of circ‐CDC45. High circ‐CDC45 expression was found in GM specimens and cells, which was tightly related to a larger tumor size, higher world health organization (WHO) stages, and worse survival for patients with GM. Functionally, manipulation of circ‐CDC45 expression strongly affected cell growth, apoptosis, migration and invasion, which suggests the oncogenic function of circ‐CDC45 in GM oncogenesis. Stepwise mechanism studies indicated that circ‐CDC45 sponged and regulated the expression of miR‐516b and miR‐527 to promote cell growth and invasion. Briefly, the regulatory network of circ‐CDC45/miR‐516b/miR‐527 plays a pivotal role in GM tumorigenesis and may act as a potential target for GM treatment.

show abstract

“…Some studies reported that circRNA might act as sponges for miRNA, regulating the expression of miRNA target genes in glioma. Wang R et al found that circNT5E could promote cell proliferation, migration, and invasion through acting as a sponge of miR-422a (Wang et al 2018b). Li X et al found that circ_0001946 acted as a competing endogenous RNA to modulating miR-671-5p and CDR1, and reduced proliferation, migration, invasion and increased apoptosis in GBM cells (Li and Diao 2019).…”

Section: Discussionmentioning

confidence: 99%

circKIF4A promotes tumorogenesis of glioma by targeting miR-139-3p to activate Wnt5a signaling

Huo

Wang

Bai

et al. 2020

Mol Med

View full text Add to dashboard Cite

Background: Glioma has the characteristics of high incidence and mortality, and is a common malignant tumor of the central nervous system. Circular RNAs (circRNAs) have been reported to play vital roles in progression of cancer including glioma, and circKIF4A is up-regulated in glioma tissues. However, its role and mechanisms in gliomas are unclear.Methods: circKIF4A and miR-139-3p were determined by qRT-PCR. Transwell assay, wound-healing assay, cell colony formation and flow cytometry were performed to measure cell invasion, migration, proliferation and apoptosis. Western blotting was used to evaluate Wnt/β-catenin pathway-related protein. Luciferase reporter assays confirmed the relationship among circKIF4A, miR-139-3p and Wnt5a. Sphere formation was performed to measure the ability of glioma-initiating cells (GICs) spheroid formation. A nude mouse xenograft model was established and immunohistochemical staining was used to detect Ki-67 and Wnt5a levels.Results: circKIF4A and Wnt5a were up-regulated and miR-139-3p was down-regulated in both glioma cells and tissues. circKIF4A promoted Wnt5a expression by sponging miR-139-3p. Knockdown of circKIF4A inhibited the colony formation ability, migration and invasion, and promoted the apoptosis of glioma cells by regulating miR-139-3p. Knockdown of circKIF4A inhibited Wnt/β-catenin signaling pathway and proliferation-related signal via miR-139-3p. Furthermore, knockdown of circKIF4A or overexpression of miR-139 suppressed the ability of sphere formation of GICs and inhibitd Wnt/β-catenin signaling pathway and proliferation-related signal in GICs. Additionally, depletion of circKIF4A decreased the expression level of Wnt5a and Ki-67, inhibited tumorigenesis in xenograft modes.Conclusion: circKIF4A was overexpressed in glioma, and knockdown of circKIF4A suppressed glioma progression via miR-139-3p/Wnt5a axis. The results indicated that circKIF4A may be a potential target for clinical treatment of glioma.

show abstract

CircNT5E Acts as a Sponge of miR-422a to Promote Glioblastoma Tumorigenesis

Cited by 249 publications

References 58 publications

Splicing Dysregulation as Oncogenic Driver and Passenger Factor in Brain Tumors

Splicing Dysregulation as Oncogenic Driver and Passenger Factor in Brain Tumors

Overexpression of circular RNA circ‐CDC45 facilitates glioma cell progression by sponging miR‐516b and miR‐527 and predicts an adverse prognosis

circKIF4A promotes tumorogenesis of glioma by targeting miR-139-3p to activate Wnt5a signaling

Contact Info

Product

Resources

About