FBXW7 Triggers Degradation of KMT2D to Favor Growth of Diffuse Large B-cell Lymphoma Cells.


Journal

Cancer research
ISSN: 1538-7445
Titre abrégé: Cancer Res
Pays: United States
ID NLM: 2984705R

Informations de publication

Date de publication:
15 06 2020
Historique:
received: 22 07 2019
revised: 25 02 2020
accepted: 21 04 2020
pubmed: 1 5 2020
medline: 11 11 2020
entrez: 1 5 2020
Statut: ppublish

Résumé

Mature B-cell neoplasms are the fifth most common neoplasm. Due to significant heterogeneity at the clinical and genetic levels, current therapies for these cancers fail to provide long-term cures. The clinical success of proteasome inhibition for the treatment of multiple myeloma and B-cell lymphomas has made the ubiquitin pathway an important emerging therapeutic target. In this study, we assessed the role of the E3 ligase FBXW7 in mature B-cell neoplasms. FBXW7 targeted the frequently inactivated tumor suppressor KMT2D for protein degradation, subsequently regulating gene expression signatures related to oxidative phosphorylation (OxPhos). Loss of FBXW7 inhibited diffuse large B-cell lymphoma cell growth and further sensitized cells to OxPhos inhibition. These data elucidate a novel mechanism of regulation of KMT2D levels by the ubiquitin pathway and uncover a role of FBXW7 in regulating oxidative phosphorylation in B-cell malignancies. SIGNIFICANCE: These findings characterize FBXW7 as a prosurvival factor in B-cell lymphoma via degradation of the chromatin modifier KMT2D.

Identifiants

pubmed: 32350066
pii: 0008-5472.CAN-19-2247
doi: 10.1158/0008-5472.CAN-19-2247
pmc: PMC7417195
mid: NIHMS1594798
doi:

Substances chimiques

Chromatin 0
DNA-Binding Proteins 0
F-Box-WD Repeat-Containing Protein 7 0
FBXW7 protein, human 0
KMT2D protein, human 0
Neoplasm Proteins 0
RNA, Small Interfering 0
Ubiquitin 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2498-2511

Subventions

Organisme : NIAMS NIH HHS
ID : K08 AR070289
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA207513
Pays : United States

Informations de copyright

©2020 American Association for Cancer Research.

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Auteurs

Rizwan Saffie (R)

Department of Cancer Biology and Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.

Nan Zhou (N)

Department of Cancer Biology and Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.

Delphine Rolland (D)

Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.

Özlem Önder (Ö)

Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.

Venkatesha Basrur (V)

Department of Pathology and Clinical Laboratories, University of Michigan, Ann Arbor, Michigan.

Sydney Campbell (S)

Department of Cancer Biology and Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.

Kathryn E Wellen (KE)

Department of Cancer Biology and Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.

Kojo S J Elenitoba-Johnson (KSJ)

Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.

Brian C Capell (BC)

Penn Epigenetics Institute, Department of Cell and Developmental Biology, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania.
Department of Dermatology, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania.

Luca Busino (L)

Department of Cancer Biology and Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania. businol@upenn.edu.

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