ArticleMolecular cancer research : MCR2015
A p53/ARF-dependent anticancer barrier activates senescence and blocks tumorigenesis without impacting apoptosis.
Article in Molecular cancer research : MCR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Senataxin Attenuates DNA Damage Response Activation and Suppresses Senescence.Antioxidants (Basel, Switzerland) · 2024Article
- Advances in Immunocompetent Mouse and Rat Models.Cold Spring Harbor perspectives in medicine · 2024Review
- Targeting the Pro-survival Protein BCL-2 to Prevent Breast Cancer.Cancer prevention research (Philadelphia, Pa.) · 2022Article
- Advances in Rodent Models for Breast Cancer Formation, Progression, and Therapeutic Testing.Frontiers in oncology · 2021Review
- Intraductal Injection of Lentivirus Vectors for Stably Introducing Genes into Rat Mammary Epithelial Cells in Vivo.Journal of mammary gland biology and neoplasia · 2020Article
- Chlorogenic acid effectively treats cancers through induction of cancer cell differentiation.Theranostics · 2019Article
- Hyperprolactinemia-inducing antipsychotics increase breast cancer risk by activating JAK-STAT5 in precancerous lesions.Breast cancer research : BCR · 2018Article
- Effect of KNDC1 overexpression on the senescence of human umbilical vein endothelial cells.Molecular medicine reports · 2018Article
- Aberrant expression of p16Cancer reports and reviews · 2018Article
- SOCS1 regulates senescence and ferroptosis by modulating the expression of p53 target genes.Aging · 2017Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledIn response to oncogene activation and oncogene-induced aberrant proliferation, mammalian cells activate apoptosis and senescence, usually via the p53-ARF tumor-suppressor pathway. Apoptosis is a known barrier to cancer and is usually downregulated before full malignancy, but senescence as an anticancer barrier is controversial due to its presence in the tumor environment. In addition, senescence may aid cancer progression via releasing senescence-associated factors that instigate neighboring tumor cells. Here, it is demonstrated that apoptosis unexpectedly remains robust in ErbB2 (ERBB2/HER2)-initiated mammary early lesions arising in adult mice null for either p53 or ARF. These early lesions, however, downregulate senescence significantly. This diminished senescence response is associated with accelerated progression to cancer in ARF-null mice compared with ARF-wild-type mice. Thus, the ARF-p53 pathway is dispensable for the apoptosis anticancer barrier in the initiation of ErbB2 breast cancer, the apoptosis barrier alone cannot halt mammary tumorigenesis, and senescence is a key barrier against carcinogenesis. IMPLICATIONS: Findings in this relevant mouse model of HER2-driven breast cancer suggest that effective prevention relies upon preserving both ARF/p53-independent apoptosis and ARF/p53-dependent senescence.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.