Aberrant regulation of developmental pathways plays a key role in tumorigenesis. Tumor cells differ from normal cells in their sustained proliferation, replicative immortality, resistance to cell death and growth inhibition, angiogenesis, and metastatic behavior. Often they acquire these features as a consequence of dysregulated Hedgehog, Notch, or WNT signaling pathways. Human tumor viruses affect the cancer cell hallmarks by encoding oncogenic proteins, and/or by modifying the microenvironment, as well as by conveying genomic instability to accelerate cancer development. In addition, viral immune evasion mechanisms may compromise developmental pathways to accelerate tumor growth. Viruses achieve this by influencing both coding and non-coding gene regulatory pathways. Elucidating how oncogenic viruses intersect with and modulate developmental pathways is crucial to understanding viral tumorigenesis. Many currently available antiviral therapies target viral lytic cycle replication but with low efficacy and severe side effects. A greater understanding of the cross-signaling between oncogenic viruses and developmental pathways will improve the efficacy of next-generation inhibitors and pave the way to more targeted antiviral therapies.

When viruses cross developmental pathways / Trivedi, P.; Patel, S. K.; Bellavia, D.; Messina, E.; Palermo, R.; Ceccarelli, S.; Marchese, C.; Anastasiadou, E.; Minter, L. M.; Felli, M. P.. - In: FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY. - ISSN 2296-634X. - 9:(2021). [10.3389/fcell.2021.691644]

When viruses cross developmental pathways

Trivedi P.;Patel S. K.;Bellavia D.;Messina E.;Palermo R.;Ceccarelli S.;Marchese C.;Anastasiadou E.
Writing – Review & Editing
;
Felli M. P.
Ultimo
Writing – Review & Editing
2021

Abstract

Aberrant regulation of developmental pathways plays a key role in tumorigenesis. Tumor cells differ from normal cells in their sustained proliferation, replicative immortality, resistance to cell death and growth inhibition, angiogenesis, and metastatic behavior. Often they acquire these features as a consequence of dysregulated Hedgehog, Notch, or WNT signaling pathways. Human tumor viruses affect the cancer cell hallmarks by encoding oncogenic proteins, and/or by modifying the microenvironment, as well as by conveying genomic instability to accelerate cancer development. In addition, viral immune evasion mechanisms may compromise developmental pathways to accelerate tumor growth. Viruses achieve this by influencing both coding and non-coding gene regulatory pathways. Elucidating how oncogenic viruses intersect with and modulate developmental pathways is crucial to understanding viral tumorigenesis. Many currently available antiviral therapies target viral lytic cycle replication but with low efficacy and severe side effects. A greater understanding of the cross-signaling between oncogenic viruses and developmental pathways will improve the efficacy of next-generation inhibitors and pave the way to more targeted antiviral therapies.
2021
hedgehog; immune evasion; microRNA; notch; oncogenic viruses; targeted therapies; WNT
01 Pubblicazione su rivista::01g Articolo di rassegna (Review)
When viruses cross developmental pathways / Trivedi, P.; Patel, S. K.; Bellavia, D.; Messina, E.; Palermo, R.; Ceccarelli, S.; Marchese, C.; Anastasiadou, E.; Minter, L. M.; Felli, M. P.. - In: FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY. - ISSN 2296-634X. - 9:(2021). [10.3389/fcell.2021.691644]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1567658
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