Consequence of the tumor‐associated conversion to cyclin D1b

Abstract Clinical evidence suggests that cyclin D1b, a variant of cyclin D1, is associated with tumor progression and poor outcome. However, the underlying molecular basis was unknown. Here, novel models were created to generate a genetic switch from cyclin D1 to cyclin D1b. Extensive analyses uncov...

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Main Authors: Michael A Augello, Lisa D Berman‐Booty, Richard Carr, Akihiro Yoshida, Jeffry L Dean, Matthew J Schiewer, Felix Y Feng, Scott A Tomlins, Erhe Gao, Walter J Koch, Jeffrey L Benovic, John Alan Diehl, Karen E Knudsen
Format: Article
Language:English
Published: Springer Nature 2015-03-01
Series:EMBO Molecular Medicine
Subjects:
Online Access:https://doi.org/10.15252/emmm.201404242
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author Michael A Augello
Lisa D Berman‐Booty
Richard Carr
Akihiro Yoshida
Jeffry L Dean
Matthew J Schiewer
Felix Y Feng
Scott A Tomlins
Erhe Gao
Walter J Koch
Jeffrey L Benovic
John Alan Diehl
Karen E Knudsen
author_facet Michael A Augello
Lisa D Berman‐Booty
Richard Carr
Akihiro Yoshida
Jeffry L Dean
Matthew J Schiewer
Felix Y Feng
Scott A Tomlins
Erhe Gao
Walter J Koch
Jeffrey L Benovic
John Alan Diehl
Karen E Knudsen
author_sort Michael A Augello
collection DOAJ
description Abstract Clinical evidence suggests that cyclin D1b, a variant of cyclin D1, is associated with tumor progression and poor outcome. However, the underlying molecular basis was unknown. Here, novel models were created to generate a genetic switch from cyclin D1 to cyclin D1b. Extensive analyses uncovered overlapping but non‐redundant functions of cyclin D1b compared to cyclin D1 on developmental phenotypes, and illustrated the importance of the transcriptional regulatory functions of cyclin D1b in vivo. Data obtained identify cyclin D1b as an oncogene, wherein cyclin D1b expression under the endogenous promoter induced cellular transformation and further cooperated with known oncogenes to promote tumor growth in vivo. Further molecular interrogation uncovered unexpected links between cyclin D1b and the DNA damage/PARP1 regulatory networks, which could be exploited to suppress cyclin D1b‐driven tumors. Collectively, these data are the first to define the consequence of cyclin D1b expression on normal cellular function, present evidence for cyclin D1b as an oncogene, and provide pre‐clinical evidence of effective methods to thwart growth of cells dependent upon this oncogenic variant.
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spelling doaj-art-c0a939ceeb9240749fd9c3c0d5d3e22e2025-08-20T03:05:55ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842015-03-017562864710.15252/emmm.201404242Consequence of the tumor‐associated conversion to cyclin D1bMichael A Augello0Lisa D Berman‐Booty1Richard Carr2Akihiro Yoshida3Jeffry L Dean4Matthew J Schiewer5Felix Y Feng6Scott A Tomlins7Erhe Gao8Walter J Koch9Jeffrey L Benovic10John Alan Diehl11Karen E Knudsen12Department of Cancer Biology, Thomas Jefferson UniversityDepartment of Cancer Biology, Thomas Jefferson UniversityKimmel Cancer Center, Thomas Jefferson UniversityMedical University of South CarolinaDepartment of Cancer Biology, Thomas Jefferson UniversityDepartment of Cancer Biology, Thomas Jefferson UniversityMichigan Center for Translational Pathology, University of Michigan Medical CenterMichigan Center for Translational Pathology, University of Michigan Medical CenterPharmacology & Center for Translational MedicinePharmacology & Center for Translational MedicineKimmel Cancer Center, Thomas Jefferson UniversityMedical University of South CarolinaDepartment of Cancer Biology, Thomas Jefferson UniversityAbstract Clinical evidence suggests that cyclin D1b, a variant of cyclin D1, is associated with tumor progression and poor outcome. However, the underlying molecular basis was unknown. Here, novel models were created to generate a genetic switch from cyclin D1 to cyclin D1b. Extensive analyses uncovered overlapping but non‐redundant functions of cyclin D1b compared to cyclin D1 on developmental phenotypes, and illustrated the importance of the transcriptional regulatory functions of cyclin D1b in vivo. Data obtained identify cyclin D1b as an oncogene, wherein cyclin D1b expression under the endogenous promoter induced cellular transformation and further cooperated with known oncogenes to promote tumor growth in vivo. Further molecular interrogation uncovered unexpected links between cyclin D1b and the DNA damage/PARP1 regulatory networks, which could be exploited to suppress cyclin D1b‐driven tumors. Collectively, these data are the first to define the consequence of cyclin D1b expression on normal cellular function, present evidence for cyclin D1b as an oncogene, and provide pre‐clinical evidence of effective methods to thwart growth of cells dependent upon this oncogenic variant.https://doi.org/10.15252/emmm.201404242cell cyclecyclincyclin D1bPARP
spellingShingle Michael A Augello
Lisa D Berman‐Booty
Richard Carr
Akihiro Yoshida
Jeffry L Dean
Matthew J Schiewer
Felix Y Feng
Scott A Tomlins
Erhe Gao
Walter J Koch
Jeffrey L Benovic
John Alan Diehl
Karen E Knudsen
Consequence of the tumor‐associated conversion to cyclin D1b
EMBO Molecular Medicine
cell cycle
cyclin
cyclin D1b
PARP
title Consequence of the tumor‐associated conversion to cyclin D1b
title_full Consequence of the tumor‐associated conversion to cyclin D1b
title_fullStr Consequence of the tumor‐associated conversion to cyclin D1b
title_full_unstemmed Consequence of the tumor‐associated conversion to cyclin D1b
title_short Consequence of the tumor‐associated conversion to cyclin D1b
title_sort consequence of the tumor associated conversion to cyclin d1b
topic cell cycle
cyclin
cyclin D1b
PARP
url https://doi.org/10.15252/emmm.201404242
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