miR-223 inhibits dengue virus replication by negatively regulating the microtubule-destabilizing protein STMN1 in EAhy926 cells

Wu, Na; Gao, Na; Fan, Dongying; Wei, Jianchun; Zhang, Jing; An, Jing

doi:10.1016/j.micinf.2014.08.011

Cited by 54 publications

(47 citation statements)

References 43 publications

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“…STMN1 is a 17-kDa cytoplasmic protein, which is also named as oncoprotein 18 (OP18) [41][42][43]. Previous research showed that STMN1 acted as an important regulator in cell cycle, proliferation, invasion and survival through regulating microtubule dynamics [44][45][46]. STMN1 was upregulated in several human tumors such as lung cancer, gastric cancer, oral squamous-cell carcinoma, colorectal tumor, gallbladder cancer and breast cancer [47][48][49][50][51].…”

Section: Discussionmentioning

confidence: 99%

miR-423-5p Inhibits Osteosarcoma Proliferation and Invasion Through Directly Targeting STMN1

Wang¹,

Peng²,

Gong³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Increasing evidences suggest that dysregulated expression of miRNAs contributes to the progression of various tumors. However, the underlying function of miR-423-5p in osteosarcoma remains unexplored. Methods: The expression of miR-423-5p and STMN1 were determined in osteosarcoma samples and cell lines via quantitative real-time PCR. Colony formation and Cell Counting Kit-8 (CCK-8) assays were performed to measure cell proliferation ability and transwell analysis was used to detect cell invasion, and dual luciferase reporter assay was perform to analysis the interaction between the miR-423-5p and STMN1. Results: The expression levels of miR-423-5p and STMN1 in the osteosarcoma tissues and cell lines were measured by qRT-PCR. Cell viability was determined using the clone formation and CCK-8 assays. A dual-luciferase reporter and Western blot were performed to stdudy the target gene of miR-423-5p. Here, we showed that miR-423-5p expression was downregulated in osteosarcoma tissues and cell lines. However, the expression of stathmin1 (STMN1) was downregulated in osteosarcoma tissues and cell lines. Moreover, STMN1 expression level was negatively correlated with the miR-423-5p expression in the osteosarcoma tissues. We identified STMN1 was a direct target gene of miR-423-5p in osteosarcoma cell. Overexpression of miR-423-5p inhibited osteosarcoma cell proliferation, colony formation and invasion. Furthermore, we demonstrated that STMN1 was involved in miR-423-5p-mediated cell behavior such as cell proliferation, colony formation and invasion in the osteosarcoma cell. Conclusion: Our present study indicated that miR-423-5p acted as a tumor suppressor gene in osteosarcoma partly through inhibiting STMN1 expression.

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Section: Discussionmentioning

confidence: 99%

miR-423-5p Inhibits Osteosarcoma Proliferation and Invasion Through Directly Targeting STMN1

Wang¹,

Peng²,

Gong³

et al. 2018

Cell Physiol Biochem

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“…Specifically, it was reported that miR-223 played a role in the pathogenesis of certain infectious diseases, such as influenza and chronic hepatitis B virus infection, and an antiviral effect for miR-223 was also observed in severe acute respiratory syndrome (SARS)-coronavirus-infected bronchoalveolar stem cells and in freshly isolated HIV-1-infected monocytes (36 -40). Furthermore, miR-223 was found to inhibit dengue virus 2 (DENV2) replication in human endothelium-like EAhy926 cells by targeting microtubule-destabilizing protein stathmin 1 (STMN1) (41). However, less is known about the detailed roles of miR-223 in the regulation of the innate antiviral response.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-223 Promotes Type I Interferon Production in Antiviral Innate Immunity by Targeting Forkhead Box Protein O3 (FOXO3)

Chen¹,

Song²,

et al. 2016

Journal of Biological Chemistry

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Effective recognition of viral infection and subsequent triggering of antiviral innate immune responses are essential for the host antiviral defense, which is tightly regulated by multiple regulators, including microRNAs. Previous reports have shown that some microRNAs are induced during virus infection and participate in the regulation of the innate antiviral response. However, whether the type I IFN response is regulated by miR-223 is still unknown. Here, we reported that vesicular stomatitis virus (VSV) infection induced significant up-regulation of miR-223 in murine macrophages. We observed that miR-223 overexpression up-regulated type I IFN expression levels in VSV-infected macrophages. We also demonstrated that miR-223 directly targets FOXO3 to regulate the type I IFN production. Furthermore, type I IFN, which is triggered by VSV infection, is responsible for the up-regulation of miR-223, thus forming a positive regulatory loop for type I IFN production. Our results uncovered a novel mechanism of miR-223-mediated regulation of type I IFN production in the antiviral innate immunity for the first time.Host innate immune response is the first line of defense following viral infection, which recognizes viral components and produces proinflammatory cytokines and interferons (1-8). The IFN family of antiviral cytokines, especially type I IFN, plays pivotal roles in the host antiviral innate immune response. They are known to inhibit viral replication and mediate protection against viral infection (1-4). Type I IFN production during virus infection should be tightly controlled by multiple intracellular regulators to initiate an appropriate immune response for eliminating the invading pathogens and preventing the development of immunopathological conditions; principal among these is the family of interferon regulatory factors (9 -12). Among the interferon regulatory factors, IRF3 and IRF7 are crucial in the host response to virus infection, inducing the transcription of the type I IFN genes, including the Ifn-␤ gene as well as a number of Ifn-␣ genes (13-16). It has been reported that IRF7 is regulated at three different levels, including the transcriptional, post-transcriptional, and post-translational levels. Transcription of the Irf7 gene is induced by viral infection or type I IFN stimulation (17), although the stability of IRF7 is regulated by FOXO3 (18).MicroRNAs (miRNAs) 4 are small, non-coding, regulatory RNAs that range from 18 to 22 nucleotides in length. They are mainly encoded by gene introns but are also sometimes encoded by dedicated genes. The miRNAs regulate the expression of specific target proteins by either inhibiting translation or degrading the corresponding mRNA (19,20). They regulate between one-and two-thirds of the human genome and participate in most of the cell's main functions (including growth, proliferation, differentiation, signal transduction, apoptosis, metabolism, and aging) (21). It has been reported that, with respect to virus infection, miRNAs constitute a critical additional c...

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“…Furthermore, proviral miRNAs can promote viral infection by suppressing antiviral factors, such as interferon (IFN), allowing the virus to escape the immune response of the host (Sharma et al, 2015;Bruscella et al, 2017). In contrast, various host miRNAs can act have antiviral functions by influencing the production of viral RNA, blocking the viral replication, suppressing proviral proteins or by inducing the virus to enter a latent phase (Zheng et al, 2013;Wu et al, 2014;Slonchak et al, 2015;Ho et al, 2016).…”

Section: Classification Of Micrornas Involved In Viral Infectionsmentioning

confidence: 99%

MicroRNA Involvement in Signaling Pathways During Viral Infection

Barbu

Condrat

Thompson

et al. 2020

Front. Cell Dev. Biol.

120

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miR-223 inhibits dengue virus replication by negatively regulating the microtubule-destabilizing protein STMN1 in EAhy926 cells

Cited by 54 publications

References 43 publications

miR-423-5p Inhibits Osteosarcoma Proliferation and Invasion Through Directly Targeting STMN1

miR-423-5p Inhibits Osteosarcoma Proliferation and Invasion Through Directly Targeting STMN1

MicroRNA-223 Promotes Type I Interferon Production in Antiviral Innate Immunity by Targeting Forkhead Box Protein O3 (FOXO3)

MicroRNA Involvement in Signaling Pathways During Viral Infection

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