Cited by 140Telomeres, Telomerase, and SenescenceCancer-related Molecular PathwaysProtein Kinase Regulation and GTPase Signaling

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Rb Regulates DNA Damage Response and Cellular Senescence through E2F-Dependent Suppression of N-Ras Isoprenylation

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Shamma, Awad, Takegami, Yujiro, Miki, Takao, Kitajima, Shunsuke, Noda, Makoto, Obara, Takao, Okamoto, Takahiro, Takahashi, Chiaki·2009·Cancer Cell

DOI 10.1016/j.ccr.2009.03.001

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Abstract

Oncogene-induced cellular senescence is well documented, but little is known about how infinite cell proliferation induced by loss of tumor suppressor genes is antagonized by cellular functions. Rb heterozygous mice generate Rb-deficient C cell adenomas that progress to adenocarcinomas following biallelic loss of N-ras. Here, we demonstrate that pRb inactivation induces aberrant expression of farnesyl diphosphate synthase, many prenyltransferases, and their upstream regulators sterol regulatory element-binding proteins (SREBPs) in an E2F-dependent manner, leading to enhanced isoprenylation and activation of N-Ras. Consequently, elevated N-Ras activity induces DNA damage response and p130-dependent cellular senescence in Rb-deficient cells. Furthermore, Rb heterozygous mice additionally lacking any of Ink4a, Arf, or Suv39h1 generated C cell adenocarcinomas, suggesting that cellular senescence antagonizes Rb-deficient carcinogenesis.

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Authors: Shamma, A., Takegami, Y., Miki, T., Kitajima, S., Noda, M., Obara, T., Okamoto, T., & Takahashi, C.
Affiliations: Kyoto University (JP)
Tokyo Women's Medical University (JP)
Corresponding author: Takahashi, Chiaki
ORCID: Shamma, Awad
Kitajima, Shunsuke
Noda, Makoto
Okamoto, Takahiro
Takahashi, Chiaki
Venue: Cancer Cell
Publisher: Elsevier BV
Published: 2009-04
Volume: 15
Issue: 4
Pages: 255-269
ISSN: 1535-6108 (ISSN-L)
DOI: 10.1016/j.ccr.2009.03.001
OpenAlex: W2122846804
Cited by: 140
References: 63
Citations by year: 2026: 1 · 2025: 4 · 2024: 8 · 2023: 5 · 2022: 6 · 2021: 14 · 2020: 10 · 2019: 12 · 2018: 5 · 2017: 7 · 2016: 10 · 2015: 11 · 2014: 11 · 2013: 9 · 2012: 7
FWCI: 5.96
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 1568 d)
Locations: Cancer Cell (publishedVersion)
PubMed (publishedVersion)
Institutional Repositories DataBase (IRDB) (submittedVersion)
Institutional Repositories DataBase (IRDB) (submittedVersion, cc-by-nc-nd)
Kanazawa University Repository for Academic Resources (DSpace) (Kanazawa University) (submittedVersion, cc-by-nc-nd)
Kyoto University Research Information Repository (Kyoto University) (submittedVersion)
Funders: Princess Takamatsu Cancer Research Fund
Takeda Science Foundation
Ministry of Education, Culture, Sports, Science and Technology
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Keywords: retinoblastoma protein, oncogene-induced senescence, NRAS, isoprenylation, DNA damage response, E2F transcription factors, farnesyl diphosphate synthase, prenyltransferase, SREBP, p130, INK4A, ARF, SUV39H1, tumor suppressor inactivation, carcinogenesis
MeSH terms: Adenocarcinoma, Adenoma, Animals, Cell Membrane, DNA Damage, DNA Repair, Humans, Immunoenzyme Techniques, Genes, ras, Thyroid Neoplasms, Retinoblastoma Protein, Cellular Senescence, Protein Prenylation, Mice, Knockout, Cyclin-Dependent Kinase Inhibitor p16, Brain Stem Neoplasms, Protein Transport, Chromatin Immunoprecipitation, E2F Transcription Factors, Mice, Prenylation

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Rb Regulates DNA Damage Response and Cellular Senescence through E2F-Dependent Suppression of N-Ras Isoprenylation

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