Avian leukosis virus subgroup J induces VEGF expression <i>via</i> NF-κB/PI3K-dependent IL-6 production

Gao, Yanni; Zhang, Yao; Yao, Yongxiu; Guan, Xi‐Wen; Liu, Yongzhen; Qi, Xiaole; Wang, Yongqiang; Liu, Changjun; Zhang, Yanping; Gao, Honglei; Nair, Venugopal; Wang, Xiaomei; Gao, Yulong

doi:10.18632/oncotarget.13282

Cited by 11 publications

(4 citation statements)

References 72 publications

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“…Different blood vessel growth factors and cytokines, such as VEGF, bFGF, and transforming growth factor-β (TGF-β), regulate angiogenesis and cancer angiogenesis. Targeting of their expression, secretion, or functions have been researched as novel strategies for anti-angiogenesis therapy for different human cancers [ 24 , 25 ]. However, to date, the clinical trial data are elusive [ 26 ] e.g., Avastin is an anti-VEGF inhibitor, and was approved by the US FDA in 2004 as an anti-angiogenesis drug to control breast cancer treatment.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of MALAT1 expression inhibits HUVEC proliferation by upregulation of miR-320a and downregulation of FOXM1 expression

Sun

Zhao

et al. 2017

Oncotarget

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Regulation of cancer angiogenesis could be a useful strategy in cancer therapy. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA (lncRNA), and can induce cancer cell proliferation, while lncRNAs, generally are able to act as microRNA (miRNA) sponges. The latter is a type of competitive endogenous RNA (ceRNA) that regulates expression of the targeting miRNAs and protein-coding genes. This study investigated the proliferative role of MALAT1 in human umbilical vein endothelial cells (HUVECs) and the underlying molecular events. The data showed that knockdown of MALAT1 expression using MALAT1 siRNA inhibited HUVEC proliferation and also significantly decreased levels of FOXM1 mRNA and protein in vitro, while knockdown of FOXM1 expression reduced HUVEC proliferation. Annotation of HUVEC microarray data revealed that seven miRNAs, including miR-320a, were upregulated after knockdown of MALAT1 expression in HUVECs. MALAT1 was shown to reciprocally interact with miR-320a, i.e., expression of one negatively regulated levels of the other, whereas knockdown of MALAT1 expression promoted miR-320a levels. Furthermore, miR-320a could directly target and inhibit FOXM1 expression in HUVECs. Knockdown of MALAT1 expression enhanced miR-320a expression but reduced FOXM1 expression resulting in downregulation of HUVEC proliferation. However, such an effect was inhibited by miR-320a depletion. In conclusion, this study demonstrates that miR-320a plays an important role in mediating the effects of MALAT1 on HUVEC proliferation by suppression of FOXM1 expression. Thus, targeting of this gene pathway could be a novel strategy in cancer therapy.

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Section: Discussionmentioning

confidence: 99%

Knockdown of MALAT1 expression inhibits HUVEC proliferation by upregulation of miR-320a and downregulation of FOXM1 expression

Sun

Zhao

et al. 2017

Oncotarget

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“…Previous studies have shown that both NF-κB and EGFR signaling pathways could be activated by single-infecting ALV-J or REV. For instant, ALV-J induces VEGF expression via NF-κB/PI3K-dependent IL-6 production to promote tumorigenesis (52-54). In ALV-induced erythroblastosis, c-erbB encodes the carboxyl-terminal domain of the epidermal growth factor receptor (55, 56).…”

Section: Discussionmentioning

confidence: 99%

ALV-J and REV synergistically activate a new oncogene of KIAA1199 via NF-κB and EGFR signaling regulated by miR-147

Zhou

Xue

Zhuang

et al. 2018

Preprint

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22The tumorigenesis is the result of the accumulation of multiple oncogenes and tumor 23 suppressor genes changes. Co-infection of avian leucosis virus subgroup J (ALV-J) 24 and reticuloendotheliosis virus ( REV) , as two oncogenic retroviruses, showed 25 synergistic pathogenic effects characterized by enhanced tumor initiation and 26 progression. The molecular mechanism underlying synergistic effects of ALV-J and 27 REV on the neoplasia remains unclear. Here, we found co-infection of ALV-J and 28 REV enhanced the ability of virus infection, increased viral life cycle, maintained cell 29 survival and enhanced tumor formation. We combined the high-throughput proteomic 30 readout with a large-scale miRNA screening to identify which molecules are involved 31 in the synergism. Our results revealed co-infection of ALV-J and REV activated a 32 latent oncogene of KIAA1199 and inhibited the expression of tumor suppressor miR-33 147. Further, enhanced KIAA1199, down-regulated miR-147, activated NF-κB and 34 EGFR were demonstrated in co-infected tissues and tumor. Mechanistically, we 35 showed ALV-J and REV synergistically enhanced KIAA1199 by activation of NF-κB 36 and EGFR signalling pathway, and the suppression of tumor suppressor miR-147 37 was contributed to maintain the NF-κB/KIAA1199/EGFR pathway crosstalk by 38 targeting the 3'UTR region sequences of NF-κB p50 and KIAA1199. Our results 39 contributed to the understanding of the molecular mechanisms of viral synergistic 40 tumorgenesis, which provided the evidence that suggested the synergistic actions of 41 two retroviruses could result in activation of latent pro-oncogenes. 42 Author summary 3 43The tumorigenesis is the result of the accumulation of multiple oncogenes and tumor 44 suppressor genes changes. Co-infection with ALV-J and REV showed synergistic 45 pathogenic effects characterized by enhanced tumor progression, however, the 46 molecular mechanism on the neoplasia remains unclear. Our results revealed co-47 infection of ALV-J and REV promotes tumorigenesis by both induction of a latent 48 oncogene of KIAA1199 and suppression of the expression of tumor suppressor miR-49 147. Mechanistic studies revealed that ALV-J and REV synergistically enhance 50 KIAA1199 by activation of NF-κB and EGFR signalling pathway, and the suppression 51 of tumor suppressor miR-147 was contributed to maintain the NF-52 κB/KIAA1199/EGFR pathway crosstalk by targeting the 3'UTR region sequences of 53 NF-κB p50 and KIAA1199. These results provided the evidence that suggested the 54 synergistic actions of two retroviruses could result in activation of latent pro-55 oncogenes, indicating the potential preventive target and predictive factor for ALV-J 56 and REV induced tumorigenesis. 57 Introduction 58 Viral synergism occurs commonly in the nature when co-infection of two or more 59 unrelated viruses invades the same host. As two oncogenic retroviruses, avian 60 leukosis virus subgroup J (ALV-J) and reticuloendotheliosis virus (REV) are the 61 optimal model to study the synergisti...

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“…Similarly, inhibition of the ERK/MAPK pathway suppressed ALV-A and ALV-B replication ( 73 ). Additionally, viral protein gp85 and p27 increase the production of IL-6 through activating the NF-κB/PI3K pathway and then induces the expression of vascular endothelial growth factor (VEGF)-A and its receptor VEGFR-2 in vascular endothelial cells and embryonic vascular tissue, promoting tumorigenesis ( 74 ).…”

Section: Cellular Factors Affecting Alv Replicationmentioning

confidence: 99%

Avian Leucosis Virus-Host Interaction: The Involvement of Host Factors in Viral Replication

Táng

Chang

et al. 2022

Front. Immunol.

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Avian leukosis virus (ALV) causes various diseases associated with tumor formation and decreased fertility. Moreover, ALV induces severe immunosuppression, increasing susceptibility to other microbial infections and the risk of failure in subsequent vaccination against other diseases. There is growing evidence showing the interaction between ALV and the host. In this review, we will survey the present knowledge of the involvement of host factors in the important molecular events during ALV infection and discuss the futuristic perspectives from this angle.

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Avian leukosis virus subgroup J induces VEGF expression via NF-κB/PI3K-dependent IL-6 production

Cited by 11 publications

References 72 publications

Knockdown of MALAT1 expression inhibits HUVEC proliferation by upregulation of miR-320a and downregulation of FOXM1 expression

Knockdown of MALAT1 expression inhibits HUVEC proliferation by upregulation of miR-320a and downregulation of FOXM1 expression

ALV-J and REV synergistically activate a new oncogene of KIAA1199 via NF-κB and EGFR signaling regulated by miR-147

Avian Leucosis Virus-Host Interaction: The Involvement of Host Factors in Viral Replication

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