Oncogenic Role of Fusion-circRNAs Derived from Cancer-Associated Chromosomal Translocations

Jlenia Guarnerio; Marco Bezzi; Jong Cheol Jeong; Stella V. Paffenholz; Kelsey Berry; Matteo M. Naldini; Francesco Lo-Coco; Yvonne Tay; Andrew H. Beck; Pier Paolo Pandolfi

doi:10.1016/j.cell.2016.03.020

Oncogenic Role of Fusion-circRNAs Derived from Cancer-Associated Chromosomal Translocations

Jlenia Guarnerio, Marco Bezzi, Jong Cheol Jeong, Stella V. Paffenholz, Kelsey Berry, Matteo M. Naldini, Francesco Lo-Coco, Yvonne Tay, Andrew H. Beck, Pier Paolo Pandolfi

Internal Medicine

Research output: Contribution to journal › Article › peer-review

405 Scopus citations

Abstract

Chromosomal translocations encode oncogenic fusion proteins that have been proven to be causally involved in tumorigenesis. Our understanding of whether such genomic alterations also affect non-coding RNAs is limited, and their impact on circular RNAs (circRNAs) has not been explored. Here, we show that well-established cancer-associated chromosomal translocations give rise to fusion circRNAs (f-circRNA) that are produced from transcribed exons of distinct genes affected by the translocations. F-circRNAs contribute to cellular transformation, promote cell viability and resistance upon therapy, and have tumor-promoting properties in in vivo models. Our work expands the current knowledge regarding molecular mechanisms involved in cancer onset and progression, with potential diagnostic and therapeutic implications.

Original language	English
Pages (from-to)	289-302
Number of pages	14
Journal	Cell
Volume	165
Issue number	2
DOIs	https://doi.org/10.1016/j.cell.2016.03.020
State	Published - Apr 7 2016

Bibliographical note

Funding Information:
We thank Lauren Southwood and Kaitlyn Doherty for insightful editing and all members of the Pandolfi lab for critical discussion. We thank Dr. Daniel Costa for providing H3122 cell line and Dr. Mireia Castillo Martin for providing SKNEP cell line. J.G. was supported by a fellowship from American- Italian Cancer Foundation during the execution of this work. S.V.P. has been granted leave of absence from the German Cancer Research Center DKFZ, Heidelberg.

Publisher Copyright:
© 2016 Elsevier Inc.

ASJC Scopus subject areas

Biochemistry, Genetics and Molecular Biology (all)

UN SDGs

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10.1016/j.cell.2016.03.020

Cite this

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title = "Oncogenic Role of Fusion-circRNAs Derived from Cancer-Associated Chromosomal Translocations",

abstract = "Chromosomal translocations encode oncogenic fusion proteins that have been proven to be causally involved in tumorigenesis. Our understanding of whether such genomic alterations also affect non-coding RNAs is limited, and their impact on circular RNAs (circRNAs) has not been explored. Here, we show that well-established cancer-associated chromosomal translocations give rise to fusion circRNAs (f-circRNA) that are produced from transcribed exons of distinct genes affected by the translocations. F-circRNAs contribute to cellular transformation, promote cell viability and resistance upon therapy, and have tumor-promoting properties in in vivo models. Our work expands the current knowledge regarding molecular mechanisms involved in cancer onset and progression, with potential diagnostic and therapeutic implications.",

author = "Jlenia Guarnerio and Marco Bezzi and Jeong, {Jong Cheol} and Paffenholz, {Stella V.} and Kelsey Berry and Naldini, {Matteo M.} and Francesco Lo-Coco and Yvonne Tay and Beck, {Andrew H.} and Pandolfi, {Pier Paolo}",

note = "Funding Information: We thank Lauren Southwood and Kaitlyn Doherty for insightful editing and all members of the Pandolfi lab for critical discussion. We thank Dr. Daniel Costa for providing H3122 cell line and Dr. Mireia Castillo Martin for providing SKNEP cell line. J.G. was supported by a fellowship from American- Italian Cancer Foundation during the execution of this work. S.V.P. has been granted leave of absence from the German Cancer Research Center DKFZ, Heidelberg. Publisher Copyright: {\textcopyright} 2016 Elsevier Inc.",

year = "2016",

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doi = "10.1016/j.cell.2016.03.020",

language = "English",

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AU - Guarnerio, Jlenia

AU - Bezzi, Marco

AU - Jeong, Jong Cheol

AU - Paffenholz, Stella V.

AU - Berry, Kelsey

AU - Naldini, Matteo M.

AU - Lo-Coco, Francesco

AU - Tay, Yvonne

AU - Beck, Andrew H.

AU - Pandolfi, Pier Paolo

N1 - Funding Information: We thank Lauren Southwood and Kaitlyn Doherty for insightful editing and all members of the Pandolfi lab for critical discussion. We thank Dr. Daniel Costa for providing H3122 cell line and Dr. Mireia Castillo Martin for providing SKNEP cell line. J.G. was supported by a fellowship from American- Italian Cancer Foundation during the execution of this work. S.V.P. has been granted leave of absence from the German Cancer Research Center DKFZ, Heidelberg. Publisher Copyright: © 2016 Elsevier Inc.

PY - 2016/4/7

Y1 - 2016/4/7

N2 - Chromosomal translocations encode oncogenic fusion proteins that have been proven to be causally involved in tumorigenesis. Our understanding of whether such genomic alterations also affect non-coding RNAs is limited, and their impact on circular RNAs (circRNAs) has not been explored. Here, we show that well-established cancer-associated chromosomal translocations give rise to fusion circRNAs (f-circRNA) that are produced from transcribed exons of distinct genes affected by the translocations. F-circRNAs contribute to cellular transformation, promote cell viability and resistance upon therapy, and have tumor-promoting properties in in vivo models. Our work expands the current knowledge regarding molecular mechanisms involved in cancer onset and progression, with potential diagnostic and therapeutic implications.

AB - Chromosomal translocations encode oncogenic fusion proteins that have been proven to be causally involved in tumorigenesis. Our understanding of whether such genomic alterations also affect non-coding RNAs is limited, and their impact on circular RNAs (circRNAs) has not been explored. Here, we show that well-established cancer-associated chromosomal translocations give rise to fusion circRNAs (f-circRNA) that are produced from transcribed exons of distinct genes affected by the translocations. F-circRNAs contribute to cellular transformation, promote cell viability and resistance upon therapy, and have tumor-promoting properties in in vivo models. Our work expands the current knowledge regarding molecular mechanisms involved in cancer onset and progression, with potential diagnostic and therapeutic implications.

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Oncogenic Role of Fusion-circRNAs Derived from Cancer-Associated Chromosomal Translocations

Abstract

Bibliographical note

ASJC Scopus subject areas

UN SDGs

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