Oncogenic herpesvirus KSHV triggers hallmarks of alternative lengthening of telomeres

To achieve replicative immortality, cancer cells must activate telomere maintenance mechanisms to prevent telomere shortening. ~85% of cancers circumvent telomeric attrition by re-expressing telomerase, while the remaining ~15% of cancers induce alternative lengthening of telomeres (ALT), which reli...

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Published inNature communications Vol. 12; no. 1; pp. 512 - 11
Main Authors Lippert, Timothy P., Marzec, Paulina, Idilli, Aurora I., Sarek, Grzegorz, Vancevska, Aleksandra, Bower, Mark, Farrell, Paul J., Ojala, Päivi M., Feldhahn, Niklas, Boulton, Simon J.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 21.01.2021
Nature Publishing Group
Nature Portfolio
Subjects
13
13/1
13/106
14
14/1
14/19
631/337/103/560
631/67/68
Biotechnology
Cancer
Carcinogenesis
Cell Line
Cell Line, Tumor
DNA Damage
DNA Replication - genetics
HeLa Cells
Herpes viruses
Herpesvirus 8, Human - physiology
Host-Pathogen Interactions
Humanities and Social Sciences
Humans
In Situ Hybridization, Fluorescence
Infections
Kaposi's sarcoma
Latency
Maintenance
multidisciplinary
Neoplasms - genetics
Neoplasms - pathology
Neoplasms - virology
Proteome - genetics
Proteome - metabolism
Recombination
Sarcoma
Science
Science (multidisciplinary)
Telomerase
Telomerase - genetics
Telomerase - metabolism
Telomere - genetics
Telomere Homeostasis - genetics
Telomere Shortening - genetics
Telomeres
Tumors
Yeast
Online AccessGet full text

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Abstract To achieve replicative immortality, cancer cells must activate telomere maintenance mechanisms to prevent telomere shortening. ~85% of cancers circumvent telomeric attrition by re-expressing telomerase, while the remaining ~15% of cancers induce alternative lengthening of telomeres (ALT), which relies on break-induced replication (BIR) and telomere recombination. Although ALT tumours were first reported over 20 years ago, the mechanism of ALT induction remains unclear and no study to date has described a cell-based model that permits the induction of ALT. Here, we demonstrate that infection with Kaposi’s sarcoma herpesvirus (KSHV) induces sustained acquisition of ALT-like features in previously non-ALT cell lines. KSHV-infected cells acquire hallmarks of ALT activity that are also observed in KSHV-associated tumour biopsies. Down-regulating BIR impairs KSHV latency, suggesting that KSHV co-opts ALT for viral functionality. This study uncovers KSHV infection as a means to study telomere maintenance by ALT and reveals features of ALT in KSHV-associated tumours. ~15% of cancers induce alternative lengthening of telomeres (ALT) to activate telomere maintenance. Here, the authors reveal that infection with Kaposi’s sarcoma herpesvirus (KSHV) induces acquisition of ALT-like features in previously non-ALT cell lines.
AbstractList To achieve replicative immortality, cancer cells must activate telomere maintenance mechanisms to prevent telomere shortening. ~85% of cancers circumvent telomeric attrition by re-expressing telomerase, while the remaining ~15% of cancers induce alternative lengthening of telomeres (ALT), which relies on break-induced replication (BIR) and telomere recombination. Although ALT tumours were first reported over 20 years ago, the mechanism of ALT induction remains unclear and no study to date has described a cell-based model that permits the induction of ALT. Here, we demonstrate that infection with Kaposi’s sarcoma herpesvirus (KSHV) induces sustained acquisition of ALT-like features in previously non-ALT cell lines. KSHV-infected cells acquire hallmarks of ALT activity that are also observed in KSHV-associated tumour biopsies. Down-regulating BIR impairs KSHV latency, suggesting that KSHV co-opts ALT for viral functionality. This study uncovers KSHV infection as a means to study telomere maintenance by ALT and reveals features of ALT in KSHV-associated tumours. ~15% of cancers induce alternative lengthening of telomeres (ALT) to activate telomere maintenance. Here, the authors reveal that infection with Kaposi’s sarcoma herpesvirus (KSHV) induces acquisition of ALT-like features in previously non-ALT cell lines.
To achieve replicative immortality, cancer cells must activate telomere maintenance mechanisms to prevent telomere shortening. ~85% of cancers circumvent telomeric attrition by re-expressing telomerase, while the remaining ~15% of cancers induce alternative lengthening of telomeres (ALT), which relies on break-induced replication (BIR) and telomere recombination. Although ALT tumours were first reported over 20 years ago, the mechanism of ALT induction remains unclear and no study to date has described a cell-based model that permits the induction of ALT. Here, we demonstrate that infection with Kaposi’s sarcoma herpesvirus (KSHV) induces sustained acquisition of ALT-like features in previously non-ALT cell lines. KSHV-infected cells acquire hallmarks of ALT activity that are also observed in KSHV-associated tumour biopsies. Down-regulating BIR impairs KSHV latency, suggesting that KSHV co-opts ALT for viral functionality. This study uncovers KSHV infection as a means to study telomere maintenance by ALT and reveals features of ALT in KSHV-associated tumours.~15% of cancers induce alternative lengthening of telomeres (ALT) to activate telomere maintenance. Here, the authors reveal that infection with Kaposi’s sarcoma herpesvirus (KSHV) induces acquisition of ALT-like features in previously non-ALT cell lines.
Abstract To achieve replicative immortality, cancer cells must activate telomere maintenance mechanisms to prevent telomere shortening. ~85% of cancers circumvent telomeric attrition by re-expressing telomerase, while the remaining ~15% of cancers induce alternative lengthening of telomeres (ALT), which relies on break-induced replication (BIR) and telomere recombination. Although ALT tumours were first reported over 20 years ago, the mechanism of ALT induction remains unclear and no study to date has described a cell-based model that permits the induction of ALT. Here, we demonstrate that infection with Kaposi’s sarcoma herpesvirus (KSHV) induces sustained acquisition of ALT-like features in previously non-ALT cell lines. KSHV-infected cells acquire hallmarks of ALT activity that are also observed in KSHV-associated tumour biopsies. Down-regulating BIR impairs KSHV latency, suggesting that KSHV co-opts ALT for viral functionality. This study uncovers KSHV infection as a means to study telomere maintenance by ALT and reveals features of ALT in KSHV-associated tumours.
To achieve replicative immortality, cancer cells must activate telomere maintenance mechanisms to prevent telomere shortening. ~85% of cancers circumvent telomeric attrition by re-expressing telomerase, while the remaining ~15% of cancers induce alternative lengthening of telomeres (ALT), which relies on break-induced replication (BIR) and telomere recombination. Although ALT tumours were first reported over 20 years ago, the mechanism of ALT induction remains unclear and no study to date has described a cell-based model that permits the induction of ALT. Here, we demonstrate that infection with Kaposi's sarcoma herpesvirus (KSHV) induces sustained acquisition of ALT-like features in previously non-ALT cell lines. KSHV-infected cells acquire hallmarks of ALT activity that are also observed in KSHV-associated tumour biopsies. Down-regulating BIR impairs KSHV latency, suggesting that KSHV co-opts ALT for viral functionality. This study uncovers KSHV infection as a means to study telomere maintenance by ALT and reveals features of ALT in KSHV-associated tumours.
~15% of cancers induce alternative lengthening of telomeres (ALT) to activate telomere maintenance. Here, the authors reveal that infection with Kaposi’s sarcoma herpesvirus (KSHV) induces acquisition of ALT-like features in previously non-ALT cell lines.
ArticleNumber 512
Author Marzec, Paulina
Ojala, Päivi M.
Boulton, Simon J.
Feldhahn, Niklas
Sarek, Grzegorz
Vancevska, Aleksandra
Farrell, Paul J.
Idilli, Aurora I.
Lippert, Timothy P.
Bower, Mark
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Snippet To achieve replicative immortality, cancer cells must activate telomere maintenance mechanisms to prevent telomere shortening. ~85% of cancers circumvent...
Abstract To achieve replicative immortality, cancer cells must activate telomere maintenance mechanisms to prevent telomere shortening. ~85% of cancers...
~15% of cancers induce alternative lengthening of telomeres (ALT) to activate telomere maintenance. Here, the authors reveal that infection with Kaposi’s...
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SubjectTerms 13
13/1
13/106
14
14/1
14/19
631/337/103/560
631/67/68
Biotechnology
Cancer
Carcinogenesis
Cell Line
Cell Line, Tumor
DNA Damage
DNA Replication - genetics
HeLa Cells
Herpes viruses
Herpesvirus 8, Human - physiology
Host-Pathogen Interactions
Humanities and Social Sciences
Humans
In Situ Hybridization, Fluorescence
Infections
Kaposi's sarcoma
Latency
Maintenance
multidisciplinary
Neoplasms - genetics
Neoplasms - pathology
Neoplasms - virology
Proteome - genetics
Proteome - metabolism
Recombination
Sarcoma
Science
Science (multidisciplinary)
Telomerase
Telomerase - genetics
Telomerase - metabolism
Telomere - genetics
Telomere Homeostasis - genetics
Telomere Shortening - genetics
Telomeres
Tumors
Yeast
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Title Oncogenic herpesvirus KSHV triggers hallmarks of alternative lengthening of telomeres
URI https://link.springer.com/article/10.1038/s41467-020-20819-4
https://www.ncbi.nlm.nih.gov/pubmed/33479235
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https://pubmed.ncbi.nlm.nih.gov/PMC7820467
https://doaj.org/article/10dff1fa37054d0fb9e5c512d4b0b3e9
Volume 12
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