Human cytomegalovirus infection induces transcription and secretion of transforming growth factor beta 1

Michelson, Susan; Alcamı́, José; Kim, S. J.; Danielpour, David; Bachelerie, Françoise; Picard, Laurent; Bessia, Christine; Payá, Carlos V.; Virelizier, J L

doi:10.1128/jvi.68.9.5730-5737.1994

Cited by 136 publications

(66 citation statements)

References 46 publications

(38 reference statements)

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“…87 CMV increases in vitro expression of TGF-β mRNA and protein from infected astrocytes, fibroblasts, and osteosarcoma cells. [87][88][89] Furthermore, in vitro transient expression of the CMV immediate early 1 and 2 (IE1, IE2) genes also induces TGF-β expression. 88,90 For instance, the IE2 stimulates TGF-β expression in human glioma cells, via interacting with the Egr-1 DNA-binding protein.…”

Section: Cytomegalovirusmentioning

confidence: 99%

“…[87][88][89] Furthermore, in vitro transient expression of the CMV immediate early 1 and 2 (IE1, IE2) genes also induces TGF-β expression. 88,90 For instance, the IE2 stimulates TGF-β expression in human glioma cells, via interacting with the Egr-1 DNA-binding protein. 90 Additionally, CMV also augments the FIGURE 8 A schematic illustration of the major SARS-CoV proteins and corresponding targets, by which the virus modulates the TGF-β signaling pathway FIGURE 9 A schematic illustration of the major influenza A proteins and corresponding targets, by which the virus modulates the TGF-β signaling pathway 28 -suppressed TGF-β-induced p21 expression by acting through the TGF-β-responsive element (TβRE) positioned in the p21 promoter region.…”

Section: Cytomegalovirusmentioning

confidence: 99%

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Viruses as key modulators of the TGF‐β pathway; a double‐edged sword involved in cancer

Mirzaei

Faghihloo

2018

Reviews in Medical Virology

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Transforming growth factor-β (TGF-β) signaling pathway is a key network in cell signaling that controls vital processes such as proliferation, differentiation, apoptosis, epithelial-mesenchymal transition, and migration, thus acting as a double-edged sword in normal development and diseases, in particular organ fibrosis, vascular disorders, and cancer. Early in tumorigenesis, the pathway exerts anti-tumor effects through suppressing cell cycle and inducing apoptosis, while during late stages, it functions as a tumor promoter by enhancing tumor invasiveness and metastasis. This signaling pathway can be perturbed by environmental and genetic factors such as microbial interference and mutation, respectively. In this way, the present review describes the modulation of the TGF-β pathway by oncogenic human viral pathogens and other viruses. The main mechanisms by which viruses interferes with TGF-β signaling seems to be through (1) the alteration of either TGF-β protein expression or activation, (2) the modulation of the TGF-β receptors or SMADs factors (by interfering with their levels and functions), (3) the alteration of none-SMAD pathways, and (4) indirect interaction with the pathway by the modulation of transcriptional co-activator/repressor and regulators of the pathway. Given the axial role of this pathway in tumorigenesis, it can be regarded as an attractive target for cancer therapy. Hence, further investigations on this subject may represent molecular targets among either TGF-β signaling molecules or viral factors for the treatment and management of viral infection consequences such as cancer.

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Section: Cytomegalovirusmentioning

confidence: 99%

Section: Cytomegalovirusmentioning

confidence: 99%

Viruses as key modulators of the TGF‐β pathway; a double‐edged sword involved in cancer

Mirzaei

Faghihloo

2018

Reviews in Medical Virology

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“…20 Furthermore, it increases the production of transforming growth factor (TGF), which suppresses the immune system through several mechanisms, most notably the suppression of cytotoxic T lymphocyte and natural killer cells and counteracting IL-2 and tumor necrosis factor (TNF). 21 Also, different CMV proteins have been shown to suppress the apoptotic anti-viral response induced by TNF. 17,22 Recently, infection with CMV was reported to disrupt the function of the JAK-STAT signal transduction pathway as CMV rapidly decreases the level of Jak-1 by enhanced protein degradation in CMV-infected fibroblasts.…”

Section: Introductionmentioning

confidence: 99%

Human cytomegalovirus infection inhibits response of chronic hepatitis‐C‐virus‐infected patients to interferon‐based therapy

Din

El-Meguid

Tabll

et al. 2010

J of Gastro and Hepatol

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“…This 72-kDa phosphoprotein is abundantly expressed immediately after infection (Plachter et al, 1996). In transient transfection assays, IE1 has been shown to be involved in the autoregulation of its own promoter and also in the transactivation of viral and cellular promoters, alone or in concert with other viral or cellular proteins (Stenberg and Stinski, 1985;Davis et al, 1987;Tevethia et al, 1987;Cherrington and Mocarski, 1989;Sambucetti et al, 1989;Stenberg et al, 1989;Iwamoto et al, 1990;Hagemeier et al, 1992;Monick et al, 1992;Michelson et al, 1994;Margolis et al, 1995;Yurochko et al, 1995;Kim et al, 1999;Murayama et al, 2000). It was also reported that the IE1 gene product could cooperate with another IE gene product, IE2, and adenoviral E1A to transform primary baby rat kidney (BRK) cells (Shen et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Downregulation of GFAP, TSP‐1, and p53 in human glioblastoma cell line, U373MG, by IE1 protein from human cytomegalovirus

Lee

Jeon

Kim

et al. 2005

Glia

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Human cytomegalovirus (HCMV) is a member of the b-herpesvirus family, which has tropism for glial cells. It was recently reported that HCMV might play important roles in the pathogenesis of malignant glioma. In this study, we investigated the effects of the HCMV IE1 protein on the gene expression profile in the human glioblastoma cell line, U373MG by employing cDNA microarray technology. Using DNA chips containing approximately 1,000 human cDNAs, RNA samples from U373MG cells stably expressing IE1 were compared with those from the control cells lacking IE1 cDNA. Fluorescence intensities of 13 genes were significantly decreased in IE1-expressing cells, while one gene was found to be upregulated. Among these 14 genes, we chose to work further on glial fibrillary acidic protein (GFAP), thrombospondin-1 (TSP-1), and p53, because of their previously known involvement in tumorigenesis. The mRNA levels of all these genes were found to be decreased in IE1-expressing glioblastoma cells by real-time quantitative reverse transcriptionpolymerase chain reaction (RT-PCR) as well as Northern blot analysis. The decreased expression of these genes was also observed at protein levels as measured by immunocytochemistry or fluorescence-activated cell sorting (FACS) analysis. Our data strongly suggested that HCMV IE1 could modulate the expression of cellular genes that might play important roles in the pathogenesis of glial tumors. '

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Human cytomegalovirus infection induces transcription and secretion of transforming growth factor beta 1

Cited by 136 publications

References 46 publications

Viruses as key modulators of the TGF‐β pathway; a double‐edged sword involved in cancer

Viruses as key modulators of the TGF‐β pathway; a double‐edged sword involved in cancer

Human cytomegalovirus infection inhibits response of chronic hepatitis‐C‐virus‐infected patients to interferon‐based therapy

Downregulation of GFAP, TSP‐1, and p53 in human glioblastoma cell line, U373MG, by IE1 protein from human cytomegalovirus

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