Small G Rac1 is involved in replication cycle of dengue serotype 2 virus in EAhy926 cells via the regulation of actin cytoskeleton

Zhang, Jing; Wu, Na; Gao, Na; Yan, Wenli; Sheng, Ziyang; Fan, Dongying; An, Jing

doi:10.1007/s11427-016-5042-5

Cited by 17 publications

(15 citation statements)

References 37 publications

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“…The cytoskeleton has been reported to function at several stages of the replication cycle for members of the Flaviviridae family. For DENV infection, entry into host cells depends on microfilament integrity 132,133 . Additionally, the formation of viral ROs causes substantial remodelling of the intracellular endomembrane system and concomitantly alters the cytoskeletal architecture.…”

Section: Cytoskeletonmentioning

confidence: 99%

Rewiring cellular networks by members of the Flaviviridae family

et al. 2018

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Members of the Flaviviridae virus family comprise a large group of enveloped viruses with a single-strand RNA genome of positive polarity. Several genera belong to this family, including the Hepacivirus genus, of which hepatitis C virus (HCV) is the prototype member, and the Flavivirus genus, which contains both dengue virus and Zika virus. Viruses of these genera differ in many respects, such as the mode of transmission or the course of infection, which is either predominantly persistent in the case of HCV or acutely self-limiting in the case of flaviviruses. Although the fundamental replication strategy of Flaviviridae members is similar, during the past few years, important differences have been discovered, including the way in which these viruses exploit cellular resources to facilitate viral propagation. These differences might be responsible, at least in part, for the various biological properties of these viruses, thus offering the possibility to learn from comparisons. In this Review, we discuss the current understanding of how Flaviviridae viruses manipulate and usurp cellular pathways in infected cells. Specifically, we focus on comparing strategies employed by flaviviruses with those employed by hepaciviruses, and we discuss the importance of these interactions in the context of viral replication and antiviral therapies.

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Section: Cytoskeletonmentioning

confidence: 99%

Rewiring cellular networks by members of the Flaviviridae family

et al. 2018

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“…In EAhy926 cells, Rac1 has been reported to play an important role in the DENV serotype 2 (DENV2) life cycle by regulating actin reorganization. DENV2 infection induced dynamic changes in actin organization, and treatment with cytochalasin D or jasplakinolide disrupted actin dynamics, reduced DENV2 entry, and inhibited DENV2 assembly and maturation (Zhang et al 2016). Works in ECV304 cells showed that actin and Rac1 signaling are essential for DENV2 entry into and release from the host cell (Wang et al 2010).…”

Section: The Role Of Cytoskeleton In Denv-host Interactionmentioning

confidence: 99%

The Role of Host Cytoskeleton in Flavivirus Infection

Zhang

Wei

et al. 2019

Virol. Sin.

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The family of flaviviruses is one of the most medically important groups of emerging arthropod-borne viruses. Host cell cytoskeletons have been reported to have close contact with flaviviruses during virus entry, intracellular transport, replication, and egress process, although many detailed mechanisms are still unclear. This article provides a brief overview of the function of the most prominent flaviviruses-induced or-hijacked cytoskeletal structures including actin, microtubules and intermediate filaments, mainly focus on infection by dengue virus, Zika virus and West Nile virus. We suggest that virus interaction with host cytoskeleton to be an interesting area of future research.

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“…However, the underlying mechanisms of RAC1 activation in various types of cancer tend to be varied and complex (35). In our study, we further found that ectopic overexpression of the RAC1 short-3 0 UTR isoform in UCB cells dramatically increased protein expression of RAC1 by escaping from miRNA targeted repression and thus, largely up-regulating certain key targets, AKT and b-catenin-MMP9 pathways, which can potently stimulate cancer cell proliferation and invasion (36,37). These findings suggest that 3 0 UTR shortening of RAC1 in UCB is a critical mechanism to upregulate RAC1 expression and consequently promote UCBs tumorigenesis and/or progression.…”

Section: Discussionmentioning

confidence: 51%

CSTF2-Induced Shortening of the RAC1 3′UTR Promotes the Pathogenesis of Urothelial Carcinoma of the Bladder

et al. 2018

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Shortening of the 3' untranslated regions (3'UTR) of mRNA is an important mechanism for oncogene activation. However, 3'UTR alteration events, their pathologic functions, and underlying mechanisms in human urothelial carcinoma of the bladder (UCB) are not clear. Here, we combine RNA sequencing, bioinformatics, and clinical studies in two independent cohorts of patients with UCB to identify a novel shorter 3'UTR isoform that is frequently expressed in UCB and is critical in the tumorigenesis and acquisition of a poor prognostic phenotype in patients. Short 3'UTR isoform of substantially upregulated RAC1 expression by escaping from miRNA-targeted repression and played an essential oncogenic role in UCB pathogenesis. An important cleavage/polyadenylation factor, cleavage stimulation factor 2 (CSTF2), induced 3'UTR shortening of in UCB by mediating slow transcriptional elongation at Cotranscriptional recruitment of CSTF2 on the GUAAU motif at proximal polyadenylation site of attenuated the recruitment of two transcription factors AFF1 and AFF4, causing the defects in elongation. CSTF2 regulated the tumorigenic functions of the shorter isoform in UCB cells, enhancing cell proliferation, migration, and invasion. The combination of high expression of CSTF2 and high usage of short-3'UTR isoform may be used as a powerful biomarker to predict poor prognosis in UCB. Our findings also suggest a CSTF2-regulated-3'UTR shortening program as an exploitable therapeutic strategy for patients with UCB. These findings demonstrate that the short isoform of is critical in UCB tumorigenesis and may have implications for developing new therapeutic strategies to treat this disease..

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Small G Rac1 is involved in replication cycle of dengue serotype 2 virus in EAhy926 cells via the regulation of actin cytoskeleton

Cited by 17 publications

References 37 publications

Rewiring cellular networks by members of the Flaviviridae family

Rewiring cellular networks by members of the Flaviviridae family

The Role of Host Cytoskeleton in Flavivirus Infection

CSTF2-Induced Shortening of the RAC1 3′UTR Promotes the Pathogenesis of Urothelial Carcinoma of the Bladder

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