ArticleMolecular oncology2015
CARF (Collaborator of ARF) overexpression in p53-deficient cells promotes carcinogenesis.
Article in Molecular oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Taurine Alleviates Pancreatic β-Cell Senescence by Inhibition of p53 Pathway.Journal of diabetes · 2025Article
- CARF regulates the alternative splicing and piwi/piRNA complexes during mouse spermatogenesis through PABPC1.Acta biochimica et biophysica Sinica · 2024Article
- Cancer treatment approaches within the frame of hyperthermia, drug delivery systems, and biosensors: concepts and future potentials.RSC advances · 2024Review
- Cancer chemotherapy and beyond: Current status, drug candidates, associated risks and progress in targeted therapeutics.Genes & diseases · 2023Review
- Article
- Transcription factor p53-mediated activation of miR-519d-3p and downregulation of E2F1 attenuates prostate cancer growth and metastasis.Cancer gene therapy · 2022Article
- CDKN2AIP-induced cell senescence and apoptosis of testicular seminoma are associated with CARM1 and eIF4β.Acta biochimica et biophysica Sinica · 2022Article
- Circular RNA circFOXP1 promotes angiogenesis by regulating microRNA -127-5p/CDKN2AIP signaling pathway in osteosarcoma.Bioengineered · 2021Article
- Functional characterization of miR-708 microRNA in telomerase positive and negative human cancer cells.Scientific reports · 2021Article
- Novel Caffeic Acid Phenethyl Ester-Mortalin Antibody Nanoparticles Offer Enhanced Selective Cytotoxicity to Cancer Cells.Cancers · 2020Article
- Stress-induced changes in CARF expression determine cell fate to death, survival, or malignant transformation.Cell stress & chaperones · 2020Article
- Soyasapogenol-A targets CARF and results in suppression of tumor growth and metastasis in p53 compromised cancer cells.Scientific reports · 2020Article
- Identification of Caffeic Acid Phenethyl Ester (CAPE) as a Potent Neurodifferentiating Natural Compound That Improves Cognitive and Physiological Functions in Animal Models of Neurodegenerative Diseases.Frontiers in aging neuroscience · 2020Article
- 2, 3-Dihydro-3β-methoxy Withaferin-A Lacks Anti-Metastasis Potency: Bioinformatics and Experimental Evidences.Scientific reports · 2019Article
- CARF enrichment promotes epithelial-mesenchymal transition via Wnt/β-catenin signaling: its clinical relevance and potential as a therapeutic target.Oncogenesis · 2018Article
- Tumor suppressor activity of miR-451: Identification of CARF as a new target.Scientific reports · 2018Article
- Chemical biology reveals CARF as a positive regulator of canonical Wnt signaling by promoting TCF/β-catenin transcriptional activity.Cell discovery · 2017Article
- Article
- Loss-of-function screening to identify miRNAs involved in senescence: tumor suppressor activity of miRNA-335 and its new target CARF.Scientific reports · 2016Article
- CARF (Collaborator of ARF) overexpression in p53-deficient cells promotes carcinogenesis.Molecular oncology · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Collaborator of ARF (CARF), initially identified as a binding partner of ARF (Alternate Reading Frame), has been shown to activate ARF-p53 pathway by multiple ways including stabilization of ARF and p53 tumor suppressor proteins, and transcriptional repression of a p53 antagonist, HDM2. Level of CARF expression was shown to determine fate of cells. Whereas its knockdown caused apoptosis, its over- and super-expressions caused senescence and increase in malignant properties of cancer cells, respectively, and were closely linked to increase and decrease in p53 activity. Using p53-compromised cancer cells, we demonstrate that CARF induces growth arrest when wild type p53 is present and in p53-absence, it promotes carcinogenesis. Biochemical analyses on CARF-induced molecular signaling revealed that in p53-null cells, it caused transcriptional repression of p21(WAF1) leading to increase in CDK4, CDK6, pRb and E2F1 resulting in continued cell cycle progression. Furthermore, it instigated increase in migration and invasion of cancer cells that was marked by upregulation of MMP2, MMP3, MMP9, uPA, several interleukins and VEGF expression. Consistent with these findings, we found that human clinical samples of epithelial and glial cancers (frequently marked by loss of p53 function) possessed high level of CARF expression showing a relationship with cancer aggressiveness. The data demonstrated that CARF could be considered as a diagnostic marker and a therapeutic target in p53-compromised malignancies.
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