Rotavirus-encoded virus-like small RNA triggers autophagy by targeting IGF1R via the PI3K/Akt/mTOR pathway

Zhou, Yan; Geng, Panpan; Liu, Yalin; Wu, Jianqing; Qiao, Hai-Li; Xie, Yong; Yin, Na; Chen, Linlin; Lin, Xiaochen; Liu, Yang; Yi, Shuhua; Zhang, Guangming; Li, Hongjun; Sun, Maosheng

doi:10.1016/j.bbadis.2017.09.028

Cited by 33 publications

(34 citation statements)

References 37 publications

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“…RV-vsRNA1755 encoded by the NSP4 gene targets the host cell IGF1R which is the part of the PI3K/Akt/mTOR signaling process. In the initial stage of infection RV-vsRNA1755 activates autophagy by obstructing induction of the mTOR pathway [156].…”

Section: Dsrna Virusesmentioning

confidence: 99%

Autophagy and Viral Infection

Mao

Lin

et al. 2019

Advances in Experimental Medicine and Biology

101

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Autophagy is an intracellular recycling process that maintains cellular homeostasis by orchestrating immunity upon viral infection. Following viral infection, autophagy is often initiated to curtail infection by delivering viral particles for lysosomal degradation and further integrating with innate pattern recognition receptor signaling to induce interferon (IFN)-mediated viral clearance. However, some viruses have evolved anti-autophagy strategies to escape host immunity and to promote viral replication. In this chapter, we illustrate how autophagy prevents viral infection to generate an optimal anti-viral milieu, and then concentrate on how viruses subvert and hijack the autophagic process to evade immunosurveillance, thereby facilitating viral replication and pathogenesis. Understanding the interplays between autophagy and viral infection is anticipated to guide the development of effective anti-viral therapeutics to fight against infectious diseases.

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Section: Dsrna Virusesmentioning

confidence: 99%

Autophagy and Viral Infection

Mao

Lin

et al. 2019

Advances in Experimental Medicine and Biology

101

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“…The benefits of autophagy seem to be different for different viruses, and dependent on the time after infection. Some viruses, such as ZIKV and rotavirus require the process early in infection [43][44][45][46], whereas this is detrimental for others. Conversely, some viruses, such as influenza A virus induce autophagy late after infection to increase replication [47].…”

Section: Various Viruses Influence Autophagymentioning

confidence: 99%

Activation of the PI3K-AKT Pathway by Old World Alphaviruses

Huizen

McInerney

2020

Cells

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Alphaviruses can infect a broad range of vertebrate hosts, including birds, horses, primates, and humans, in which infection can lead to rash, fever, encephalitis, and arthralgia or arthritis. They are most often transmitted by mosquitoes in which they establish persistent, asymptomatic infections. Currently, there are no vaccines or antiviral therapies for any alphavirus. Several Old World alphaviruses, including Semliki Forest virus, Ross River virus and chikungunya virus, activate or hyperactivate the phosphatidylinositol-3-kinase (PI3K)-AKT pathway in vertebrate cells, potentially influencing many cellular processes, including survival, proliferation, metabolism and autophagy. Inhibition of PI3K or AKT inhibits replication of several alphaviruses either in vitro or in vivo, indicating the importance for viral replication. In this review, we discuss what is known about the mechanism(s) of activation of the pathway during infection and describe those effects of PI3K-AKT activation which could be of advantage to the alphaviruses. Such knowledge may be useful for the identification and development of therapies.Cells 2020, 9, 970 2 of 12 complex mTORC1. AKT signalling leads to the activation of mTORC1, which promotes cell growth by inducing lipid biogenesis through activation of the transcription factors SREBP1 and PPARγ and by promoting protein synthesis by activating the S6 kinase (S6K) and by inactivating the translational inhibitor 4E-BP1. mTORC1 also inhibits autophagy by blocking ULK1 [6]. The serine/threonine kinase glycogen synthase kinase 3 (GSK3) is another multifunctional target of AKT. Through phosphorylation, active GSK3 inhibits most of its substrates. Upon phosphorylation by AKT, GSK3 itself is inhibited and thereby the downstream targets are positively regulated. These targets include the prosurvival BCL-2 family member MCL-1 and the transcription factor c-Myc, which is required for expression of many genes involved in proliferation. Other GSK3-targets, such as glycogen synthase, are involved in (regulation of) cellular metabolism [7]. The third multifunctional target of AKT are the forkhead box O (FoxO) transcription factors. Phosphorylation of FoxO transcription factors by AKT leads to acute translocation out of the nucleus. Thus, AKT signalling suppresses the expression of FoxO targets. These include targets involved in the induction of apoptosis, cell-cycle arrest, catabolic metabolism and growth inhibition. Thus, PI3K-AKT signalling via these multifunctional targets promotes cell survival, growth and proliferation and steers cellular metabolism towards anabolism.

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“…Thus, our results suggest that 150Rik regulates MCs proliferation by acting as a molecular sponge of miR-451 to regulate the target gene IGF1R. IGF1R is a protein and transmembrane tyrosine protein receptor which is involved in the IGF1/MAPK signalling pathway [48,49]. P38MAPK, an important member of the MAPK signalling pathway, can activate the MAPK signalling pathway [50][51][52][53], causing the proliferation of cells [54][55][56].…”

Section: Discussionmentioning

confidence: 78%

The Long Noncoding RNA 150Rik Promotes Mesangial Cell Proliferation via miR-451/IGF1R/p38 MAPK Signaling in Diabetic Nephropathy

Zhang¹,

Sun²,

Peng³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Diabetic nephropathy (DN) as the primary cause of end-stage kidney disease is a common complication of diabetes. However, the initiating molecular events triggering DN are unknown. Recently, long noncoding RNAs (lncRNAs) have been shown to play important roles in DN. Methods: The expression level of lncRNA 1500026H17Rik (150Rik for short) was measured by qRT-PCR (quantitative real-time PCR). Cell proliferation ability was detected by 5-Ethynyl-2’-deoxyuridine (EdU). The relationship between 150Rik and microRNA 451 (miR-451) was examined by luciferase assay and RNA immunoprecipitation (RIP) assay. Finally, the effect of 150Rik on cell proliferation through the miR-451/insulin-like growth factor 1 receptor (IGF1R)/mitogen-activated protein kinases (p38MAPK) pathway was detected by EdU, flow cytometry analysis, western blot. Results: We found that 150Rik, an evolutionarily conserved lncRNA, was significantly upregulated in renal tissue of db/db DN mice and in mesangial cells (MCs) cultured under a high glucose condition. Further, overexpression or knockdown of 150Rik was found to regulate cell proliferation in MCs. Moreover, 150Rik was found to interact with miR-451 in both a direct and argonaute-2 (Ago2)-dependent manner. Results also revealed that overexpression of 150Rik inhibited cell proliferation through the miR-451/IGF1R/p38MAPK pathway in MCs under the high glucose condition, while knockdown of 150Rik increased cell proliferation via the miR-451/IGF1R/p38MAPK pathway. Conclusion: Taken together, these results provide new insight into the association between 150Rik and the miR-451/IGF1R/p38MAPK signaling pathway during DN progression.

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Rotavirus-encoded virus-like small RNA triggers autophagy by targeting IGF1R via the PI3K/Akt/mTOR pathway

Cited by 33 publications

References 37 publications

Autophagy and Viral Infection

Autophagy and Viral Infection

Activation of the PI3K-AKT Pathway by Old World Alphaviruses

The Long Noncoding RNA 150Rik Promotes Mesangial Cell Proliferation via miR-451/IGF1R/p38 MAPK Signaling in Diabetic Nephropathy

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