<i>Retracted</i>: Circular RNA ciRS‐7 promotes tube formation in microvascular endothelial cells through downregulation of miR‐26a‐5p

Cui, Ming; Shen, Wen; Qin, Weiwei; Wang, Xu; Li, Yanhua; Xu, Fei; Xin, Zhenlei

doi:10.1002/jbt.22468

Cited by 19 publications

(6 citation statements)

References 38 publications

(37 reference statements)

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“…CircRNAs take part in biological processes through multiple regulatory mechanism. Specifically, circRNAs are identified as competitive endogenous RNAs (ceRNAs) to sponge miRNAs, thereby attenuating the inhibitory effects of miRNAs and promoting the expression of miRNAs target genes [28]. Alternatively, circRNAs have the role of regulating gene transcription [29].…”

Section: Discussionmentioning

confidence: 99%

CircRNA circ_0004370 promotes cell proliferation, migration, and invasion and inhibits cell apoptosis of esophageal cancer via miR-1301-3p/COL1A1 axis

et al. 2021

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Background The aim of this study was to investigate the circ_0004370 expression in EC, its effects on cell proliferation, apoptosis, migration, invasion, and epithelial–mesenchymal transition (EMT) process, and the underlying regulatory mechanisms in EC. Methods The protein levels of COL1A1 and EMT-related proteins were detected by western blot. The role of circ_0004370 on cell viability, proliferation, and apoptosis was analyzed by Cell Counting Kit-8 (CCK-8) assay, colony formation assay, and flow cytometry, respectively. The transwell assay was used to examine cell migration and invasion. The binding sites between miR-1301-3p and circ_0004370 or COL1A1 were predicted by starbase software and confirmed by dual-luciferase reporter assay and RNA pull-down assay. Results We discovered that circ_0004370 was remarkably upregulated in EC tissues and cells. Knockdown of circ_0004370 inhibited cell proliferation, migration as well as invasion, and promoted apoptosis in vitro, while its effect was rescued by miR-1301-3p inhibition. And circ_0004370 mediated the EMT process in EC cells. Moreover, we explored its regulatory mechanism and found that circ_0004370 directly bound to miR-1301-3p and COL1A1 was verified as a target of miR-1301-3p. COL1A1 was highly expressed in EC cells and upregulation of COL1A1 reversed the effects of miR-1301-3p on cell proliferation, migration, invasion, and apoptosis. In addition, silencing of circ_0004370 reduced tumor volumes and weights in vivo. We showed that circ_0004370/miR-1301-3p/COL1A1 axis played the critical role in EC to regulate the cell activities. Conclusion Circ_0004370 promotes EC proliferation, migration and invasion, and EMT process and suppresses apoptosis by regulating the miR-1301-3p/COL1A1 axis, indicating that circ_0004370 may be used as a potential therapeutic target for EC.

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Section: Discussionmentioning

confidence: 99%

CircRNA circ_0004370 promotes cell proliferation, migration, and invasion and inhibits cell apoptosis of esophageal cancer via miR-1301-3p/COL1A1 axis

et al. 2021

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“…Cai et al, 2020;Meng et al, 2020). In addition, CDR1as was found to stimulate tube formation in microvascular endothelial cells by decreasing the expression of miR-26a-5p (Cui et al, 2020). Taken together, these studies demonstrate that CDR1as plays varied roles in the occurrence and development of cancer and might be a potential therapeutic target.…”

Section: Cdr1as Functions As a Mirna Spongementioning

confidence: 74%

The Emerging Picture of the Roles of CircRNA-CDR1as in Cancer

Jiang

Zeng

Shan

et al. 2020

Front. Cell Dev. Biol.

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Circular RNAs (circRNAs) are covalently closed circular structures without 5′ caps and 3′ tails, which are mainly formed from precursor mRNAs (pre-mRNAs) via back-splicing of exons. With the development of RNA sequencing and bioinformatic analysis, circRNAs were recently rediscovered and found to be widely expressed in the tree of life. Cerebellar degeneration-related protein 1 antisense RNA (CDR1as) is recognized as one of the most well-identified circRNAs. It contains over 70 miR-7 binding sites and can regulate gene activity by sponging miR-7. Increasing numbers of studies have recently demonstrated that CDR1as is abnormally expressed in many types of tumors, such as colorectal cancer, cholangiocarcinoma and osteosarcoma, and plays a vital role in the development of cancer. However, there are few reviews focusing on CDR1as and cancer. Hence, it is important to review and discuss the role of CDR1as in cancer. Here, we first review the main biological features of CDR1as. We then focus on the expression and roles of CDR1as in cancer. Finally, we summarize what is known on the role of CDR1as in cancer and discuss future prospects in this area of research.

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“…Meanwhile, miR‐26a‐5p was also regulated by other factors. MiR‐26a‐5p was downregulated by circular RNA ciRS‐7 in atherosclerosis (Cui et al, 2020). Atorvastatin (ATV) prevented atherosclerosis through miR‐26a‐5p/PTEN signaling (Jia et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

“…Meanwhile, miR-26a-5p was also regulated by other factors. MiR-26a-5p was downregulated by circular RNA ciRS-7 in atherosclerosis (Cui et al, 2020). Atorvastatin (ATV)…”

Section: Discussionmentioning

confidence: 99%

MiR‐26a‐5p alleviates cardiac hypertrophy and dysfunction via targeting ADAM17

Shi

Zhang

et al. 2021

Cell Biology International

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Cardiac hypertrophy has been a high prevalence rate throughout the world. It has posed a big threat to public health due to limited therapeutic approaches. Previous studies showed that pathological cardiac hypertrophy was associated with autophagy, microRNAs (miRNA), and other signaling pathways, while the molecular mechanisms remain incompletely characterized. In this study, we used thoracic aortic constriction (TAC)‐induced mice and angiotensin‐II (Ang‐II)‐induced H9C2 cell line as cardiac hypertrophy model to investigate the role of miR‐26a‐5p in cardiac hypertrophy. We found that miR‐26a‐5p was downregulated in cardiac hypertrophy mice. Overexpression of miR‐26a‐5p by type 9 recombinant adeno‐associated virus (rAAV9) reversed the heart hypertrophic manifestations. The phenotypes were also promoted by miR‐26a‐5p inhibitor in Ang‐II‐induced H9C2 cells. Through miRNA profile analysis and dual‐luciferase reporter assay, ADAM17 was identified as a direct target of miR‐26a‐5p. Restored expression of ADAM17 disrupted the effect of miR‐26a‐5p on cardiac hypertrophy. To sum up, these results indicated that miR‐26a‐5p played an inhibitory role in cardiac hypertrophy and dysfunction via targeting ADAM17. The miR‐26a‐5p‐ADAM17‐cardiac hypertrophy axis provided special insight and a new molecular mechanism for a better understanding of cardiac hypertrophy disease, as well as the diagnostic and therapeutic practice.

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Retracted: Circular RNA ciRS‐7 promotes tube formation in microvascular endothelial cells through downregulation of miR‐26a‐5p

Cited by 19 publications

References 38 publications

CircRNA circ_0004370 promotes cell proliferation, migration, and invasion and inhibits cell apoptosis of esophageal cancer via miR-1301-3p/COL1A1 axis

CircRNA circ_0004370 promotes cell proliferation, migration, and invasion and inhibits cell apoptosis of esophageal cancer via miR-1301-3p/COL1A1 axis

The Emerging Picture of the Roles of CircRNA-CDR1as in Cancer

MiR‐26a‐5p alleviates cardiac hypertrophy and dysfunction via targeting ADAM17

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