Identification of Potentially Functional CircRNA-miRNA-mRNA Regulatory Network in Hepatocellular Carcinoma by Integrated Microarray Analysis

Lin, Xiaoming; Chen, Yuhan

doi:10.12659/msmbr.909737

Cited by 82 publications

(64 citation statements)

References 29 publications

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“…Accumulating evidence has revealed that circRNAs could act as miRNA sponges to counteract miRNA mediated repression of mRNA [9]. Lastly, the regulatory axes of circRNAs, miRNAs, and mRNAs are gradually demonstrated in different kinds of diseases [10][11][12], including HCC [6,8]. According to previous studies, a huge number of ncRNAs, including circRNAs and miRNAs, are dysregulated in HCC [12][13][14].…”

Section: Discussionmentioning

confidence: 99%

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Circular RNA 101368/miR-200a axis modulates the migration of hepatocellular carcinoma through HMGB1/RAGE signaling

Huang

et al. 2018

Cell Cycle

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Hepatocellular carcinoma (HCC), one of the most common type of cancers, is highly refractory to most systemic therapies. Understanding the genomic dysregulations, in particularly non-coding RNA (ncRNA) dysregulations, in HCC may provide novel strategies to HCC treatment. In our previous study, we demonstrated the key role of miR-200a-mediated HMGB1/RAGE signaling in HCC carcinogenesis. In the present study, we identified circular RNA (circRNA)-miRNA pair that might modulate the migration of HCC cell lines based on previously reported GEO database (GSE78520 and GSE43445) and investigated the function and molecular mechanism. circRNA-101368 was predicted by lncTar to target miR-200a, and the expression of circRNA-101368 was significantly upregulated in HCC tissue samples; the overexpression of circRNA-101368 was correlated with poorer prognosis in patients with HCC. Moreover, circRNA-101368 knockdown suppressed the migration and the protein levels of HMGB1, RAGE and NF-κB, while increased the E-Cadherin expression in HCC cell lines. As confirmed by luciferase reporter and RNA immunoprecipitation assays, circRNA-101368 directly bound to miR-200a to negatively regulate each other. The effect of circRNA-101368 knockdown on cell migration and HMGB1/RAGE signaling could be partially attenuated by miR-200a inhibition. In tissue samples, miR-200a was negatively correlated with circRNA-101368 and HMGB1, respectively, whereas circRNA-101368 and HMGB1 was positively correlated. Taken together, we demonstrated a network of circRNAs-miRNA-mRNA in HCC and provided a novel mechanism of HCC cell migration regulation.

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Section: Discussionmentioning

confidence: 99%

“…By using integrated microarray analysis, Lin et al constructed a circRNA-miRNA-mRNA regulatory network in HCC and revealed the network might be involved in the procession of carcinogenesis of HCC. In addition, 3 top-ranked circRNAs related networks were identified to be highly correlated with the pathogenesis of HCC [8].…”

Section: Introductionmentioning

confidence: 99%

Circular RNA 101368/miR-200a axis modulates the migration of hepatocellular carcinoma through HMGB1/RAGE signaling

Huang

et al. 2018

Cell Cycle

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“…Hence, various studies have used construction of a circRNAmiRNA-mRNA interaction network to explore the functions of circRNAs [23][24][25]. The DEcircRNAmiRNA-mRNA interactions including seven DEcircRNAs (mmu_circRNA_32463, mmu_circRNA_34132 mmu_circRNA_34106, mmu_circRNA_015216, mmu_circRNA_33836, mmu_circRNA_017077 and mmu_ circRNA_003119) were predicted with Arraystar's homemade miRNA target prediction software based on TargetScan & MiRanda [26,27].…”

Section: Construction Of Decircrna-mirna-demrna Interaction Networkmentioning

confidence: 99%

The Differentially Expressed Circular RNAs in the Substantia Nigra and Corpus Striatum of Nrf2-Knockout Mice

Yang¹,

Zhang²,

Lin³

et al. 2018

Cell Physiol Biochem

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Background/Aims: The nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) pathway plays a protective role in both acute neuronal damage and chronic neurodegeneration-related oxidative stress. Circular RNAs (circRNAs) are involved with various diseases in the central nervous system (CNS). This study aimed to identify the key circRNAs involved in Nrf2-neuroprotection against oxidative stress. Methods: The differentially expressed circRNAs (DEcircRNAs) in the substantia nigra and corpus striatum between Nrf2 (-/-) and Nrf2 (+/+) mice were identified by microarray analysis. Quantitative real-time polymerase chain reaction (qRT-PCR) was then used to validate the expression of selected DEcircRNAs in the substantia nigra and corpus striatum between Nrf2 (-/-) and Nrf2 (+/+) mice. Based on our previous microarray analysis of the differentially expressed mRNAs (DEmRNAs) in the substantia nigra and corpus striatum between Nrf2 (-/-) and Nrf2 (+/+) mice, the DEcircRNA-miRNA-DEmRNA interaction network was constructed. Functional annotation of DEmRNAs that shared the same binding miRNAs with DEcircRNAs was performed using gene ontology (GO) and pathway analyses. Results: A total of 65 and 150 significant DEcircRNAs were obtained in the substantia nigra and corpus striatum of Nrf2 (-/-) mice, respectively, and seventeen shared DEcircRNAs were found in both these two tissues. The qRT-PCR results were generally consistent with the microarray results. The DEcircRNA-miRNA-DEmRNA interaction network and pathway analysis indicated that mmu_circRNA_34132, mmu_circRNA_017077 and mmu-circRNA-015216 might be involved with Nrf2-mediated neuroprotection against oxidative stress. Mmu_circRNA_015216 and mmu_circRNA_017077 might play roles in the Nrf2-related transcriptional misregulation and Nrf2-mediated processes of rheumatoid arthritis, respectively. In addition to these two processes, mmu_circRNA_34132 may be a potential regulator of Nrf2-mediated protection for diabetes mellitus and Nrf2-mediated defence against ROS in hearts. Conclusion: In conclusion, our study identified the key DEcircRNAs in the substantia nigra and corpus striatum of Nrf2 (-/-) mice, which might provide new clues for further exploring the mechanism of Nrf2-mediated neuroprotection against oxidative stress and other Nrf2-mediated processes.

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“…In conclusion, we have uncovered a novel circ_0080425–miR‐24‐3p–FGF11 axis and elaborated its importance and involvements in DN pathogenesis. Compared with advancements in cancer research (Lin & Chen, ; Rong et al, ), such evidence of ceRNAs regulation on diabetes or DN are relatively lacking. Our study provided pioneering insights and fundamental clues for future thorough understandings of the significance of noncoding RNAs on DN, which also facilitate the development of improved diagnostic and therapeutic solutions.…”

Section: Discussionmentioning

confidence: 99%

Circ_0080425 inhibits cell proliferation and fibrosis in diabetic nephropathy via sponging miR‐24‐3p and targeting fibroblast growth factor 11

Liu

Wang

et al. 2019

Journal Cellular Physiology

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Diabetic nephropathy (DN) is a severe end-stage kidney disease developed from diabetes mellitus. The involvement of circular RNAs (circRNAs) in modulating DN pathogenesis has been implied, but underlying mechanism is still lacking. In this study, we demonstrated that the expression of circ_0080425 correlated with the DN progression, and exerted positive effect on cell proliferation and fibrosis in mesangial cells. Further assessment suggested that circ_0080425 function as sponge harboring miR-24-3p. Moreover, miR-24-3p negatively correlated with the DN progression, and showed an antagonistic effect to circ_0080425on regulating MCs cell proliferation and fibrosis. Bioinformatics analysis predicted fibroblast growth factor 11 (FGF11) acting as direct downstream target of miR-24-3p. Indeed, the expression of FGF11 was significantly activated by circ_0080425 while suppressed by miR-24-3p.Knockdown of FGF11 resulted in a significant reduced cell proliferation rate and fibrosis. In addition, miR-24-3p inhibitor rescued the suppression of si-circ_0080425 on FGF11, suggesting that circ_0080425 competitive binding to miR-24-3p could release FGF11 from miR-24-3p suppression, which subsequently promoted DN progression.In conclusion, we have reported a novel circ_0080425-miR-24-3p-FGF11 axis, and explored the underlying mechanism in regulating DN pathogenesis. K E Y W O R D Scirc_0080425, diabetic nephropathy, FGF11, fibrosis, miR-24-3p

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Identification of Potentially Functional CircRNA-miRNA-mRNA Regulatory Network in Hepatocellular Carcinoma by Integrated Microarray Analysis

Cited by 82 publications

References 29 publications

Circular RNA 101368/miR-200a axis modulates the migration of hepatocellular carcinoma through HMGB1/RAGE signaling

Circular RNA 101368/miR-200a axis modulates the migration of hepatocellular carcinoma through HMGB1/RAGE signaling

The Differentially Expressed Circular RNAs in the Substantia Nigra and Corpus Striatum of Nrf2-Knockout Mice

Circ_0080425 inhibits cell proliferation and fibrosis in diabetic nephropathy via sponging miR‐24‐3p and targeting fibroblast growth factor 11

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