Oncogenic Signaling Induced by HCV Infection
The liver is frequently exposed to toxins, metabolites, and oxidative stress, which can challenge organ function and genomic stability. Liver regeneration is therefore a highly regulated process involving several sequential signaling events. It is thus not surprising that individual oncogenic mutati...
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| Format: | Article |
| Language: | English |
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MDPI AG
2018-10-01
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| Series: | Viruses |
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| Online Access: | http://www.mdpi.com/1999-4915/10/10/538 |
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| author | Alessia Virzì Armando Andres Roca Suarez Thomas F. Baumert Joachim Lupberger |
| author_facet | Alessia Virzì Armando Andres Roca Suarez Thomas F. Baumert Joachim Lupberger |
| author_sort | Alessia Virzì |
| collection | DOAJ |
| description | The liver is frequently exposed to toxins, metabolites, and oxidative stress, which can challenge organ function and genomic stability. Liver regeneration is therefore a highly regulated process involving several sequential signaling events. It is thus not surprising that individual oncogenic mutations in hepatocytes do not necessarily lead to cancer and that the genetic profiles of hepatocellular carcinomas (HCCs) are highly heterogeneous. Long-term infection with hepatitis C virus (HCV) creates an oncogenic environment by a combination of viral protein expression, persistent liver inflammation, oxidative stress, and chronically deregulated signaling events that cumulate as a tipping point for genetic stability. Although novel direct-acting antivirals (DAA)-based treatments efficiently eradicate HCV, the associated HCC risk cannot be fully eliminated by viral cure in patients with advanced liver disease. This suggests that HCV may persistently deregulate signaling pathways beyond viral cure and thereby continue to perturb cancer-relevant gene function. In this review, we summarize the current knowledge about oncogenic signaling pathways derailed by chronic HCV infection. This will not only help to understand the mechanisms of hepatocarcinogenesis but will also highlight potential chemopreventive strategies to help patients with a high-risk profile of developing HCC. |
| first_indexed | 2024-12-20T16:45:01Z |
| format | Article |
| id | doaj.art-891283001cbf4612a0f96f0b9aae68a2 |
| institution | Directory Open Access Journal |
| issn | 1999-4915 |
| language | English |
| last_indexed | 2024-12-20T16:45:01Z |
| publishDate | 2018-10-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Viruses |
| spelling | doaj.art-891283001cbf4612a0f96f0b9aae68a22022-12-21T19:32:57ZengMDPI AGViruses1999-49152018-10-01101053810.3390/v10100538v10100538Oncogenic Signaling Induced by HCV InfectionAlessia Virzì0Armando Andres Roca Suarez1Thomas F. Baumert2Joachim Lupberger3Inserm, U1110, Institut de Recherche sur les Maladies Virales et Hépatiques, 67000 Strasbourg, FranceInserm, U1110, Institut de Recherche sur les Maladies Virales et Hépatiques, 67000 Strasbourg, FranceInserm, U1110, Institut de Recherche sur les Maladies Virales et Hépatiques, 67000 Strasbourg, FranceInserm, U1110, Institut de Recherche sur les Maladies Virales et Hépatiques, 67000 Strasbourg, FranceThe liver is frequently exposed to toxins, metabolites, and oxidative stress, which can challenge organ function and genomic stability. Liver regeneration is therefore a highly regulated process involving several sequential signaling events. It is thus not surprising that individual oncogenic mutations in hepatocytes do not necessarily lead to cancer and that the genetic profiles of hepatocellular carcinomas (HCCs) are highly heterogeneous. Long-term infection with hepatitis C virus (HCV) creates an oncogenic environment by a combination of viral protein expression, persistent liver inflammation, oxidative stress, and chronically deregulated signaling events that cumulate as a tipping point for genetic stability. Although novel direct-acting antivirals (DAA)-based treatments efficiently eradicate HCV, the associated HCC risk cannot be fully eliminated by viral cure in patients with advanced liver disease. This suggests that HCV may persistently deregulate signaling pathways beyond viral cure and thereby continue to perturb cancer-relevant gene function. In this review, we summarize the current knowledge about oncogenic signaling pathways derailed by chronic HCV infection. This will not only help to understand the mechanisms of hepatocarcinogenesis but will also highlight potential chemopreventive strategies to help patients with a high-risk profile of developing HCC.http://www.mdpi.com/1999-4915/10/10/538signalingcancerHCVHCCchemopreventionliver disease |
| spellingShingle | Alessia Virzì Armando Andres Roca Suarez Thomas F. Baumert Joachim Lupberger Oncogenic Signaling Induced by HCV Infection Viruses signaling cancer HCV HCC chemoprevention liver disease |
| title | Oncogenic Signaling Induced by HCV Infection |
| title_full | Oncogenic Signaling Induced by HCV Infection |
| title_fullStr | Oncogenic Signaling Induced by HCV Infection |
| title_full_unstemmed | Oncogenic Signaling Induced by HCV Infection |
| title_short | Oncogenic Signaling Induced by HCV Infection |
| title_sort | oncogenic signaling induced by hcv infection |
| topic | signaling cancer HCV HCC chemoprevention liver disease |
| url | http://www.mdpi.com/1999-4915/10/10/538 |
| work_keys_str_mv | AT alessiavirzi oncogenicsignalinginducedbyhcvinfection AT armandoandresrocasuarez oncogenicsignalinginducedbyhcvinfection AT thomasfbaumert oncogenicsignalinginducedbyhcvinfection AT joachimlupberger oncogenicsignalinginducedbyhcvinfection |