ArticleOncogene2010
The RNA helicase p68 modulates expression and function of the Δ133 isoform(s) of p53, and is inversely associated with Δ133p53 expression in breast cancer.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- The p53 Isoforms as Potential Biomarkers in Different Cancer Entities.International journal of molecular sciences · 2026Review
- DEAD-box RNA helicases with special reference to p68: Unwinding their biology, versatility, and therapeutic opportunity in cancer.Genes & diseases · 2023Review
- DDX5 and DDX17-multifaceted proteins in the regulation of tumorigenesis and tumor progression.Frontiers in oncology · 2022Review
- Role of microRNA/lncRNA Intertwined With the Wnt/β-Catenin Axis in Regulating the Pathogenesis of Triple-Negative Breast Cancer.Frontiers in pharmacology · 2022Review
- Adaptive homeostasis and the p53 isoform network.EMBO reports · 2021Review
- The Δ133p53 Isoforms, Tuners of the p53 Pathway.Cancers · 2020Review
- The Emerging Landscape of p53 Isoforms in Physiology, Cancer and Degenerative Diseases.International journal of molecular sciences · 2019Review
- p53 and its isoforms in DNA double-stranded break repair.Journal of Zhejiang University. Science. B · 2019Review
- A functional interplay between Δ133p53 and ΔNp63 in promoting glycolytic metabolism to fuel cancer cell proliferation.Oncogene · 2018Article
- DDX5/p68 associated lncRNA LOC284454 is differentially expressed in human cancers and modulates gene expression.RNA biology · 2018Article
- Distinct modulatory role of RNA in the aggregation of the tumor suppressor protein p53 core domain.The Journal of biological chemistry · 2017Article
- Wnt signaling in triple-negative breast cancer.Oncogenesis · 2017Review
- Increased Δ133p53 mRNA in lung carcinoma corresponds with reduction of p21 expression.Molecular medicine reports · 2017Article
- Article
- p53 Isoforms: Key Regulators of the Cell Fate Decision.Cold Spring Harbor perspectives in medicine · 2016Review
- Expression of p53β and Δ133p53 isoforms in different gastric tissues.International journal of clinical and experimental pathology · 2015Article
- P68 RNA helicase as a molecular target for cancer therapy.Journal of experimental & clinical cancer research : CR · 2014Review
- The RNA helicase/transcriptional co-regulator, p68 (DDX5), stimulates expression of oncogenic protein kinase, Polo-like kinase-1 (PLK1), and is associated with elevated PLK1 levels in human breast cancers.Cell cycle (Georgetown, Tex.) · 2014Article
- Dual role of the ddx5/ddx17 RNA helicases in the control of the pro-migratory NFAT5 transcription factor.Oncogene · 2012Article
- p53 Family: Role of Protein Isoforms in Human Cancer.Journal of nucleic acids · 2012Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
The RNA helicase p68 is a potent co-activator of p53-dependent transcription in response to DNA damage. Previous independent studies have indicated that p68 and the Δ133p53 isoforms, which modulate the function of full-length p53, are aberrantly expressed in breast cancers. Here we identify a striking inverse association of p68 and Δ133p53 expression in primary breast cancers. Consistent with these findings, small interfering RNA depletion of p68 in cell lines results in a p53-dependant increase of Δ133p53 in response to DNA damage, suggesting that increased Δ133p53 expression could result from downregulation of p68 and provide a potential mechanistic explanation for our observations in breast cancer. Δ133p53α, which has been shown to negatively regulate the function of full-length p53, reciprocally inhibits the ability of p68 to stimulate p53-dependent transcription from the p21 promoter, suggesting that Δ133p53α may be competing with p68 to regulate p53 function. This hypothesis is underscored by our observations that p68 interacts with the C-terminal domain of p53, co-immunoprecipitates 133p53α from cell extracts and interacts only with p53 molecules that are able to form tetramers. These data suggest that p68, p53 and 133p53α may form part of a complex feedback mechanism to regulate the expression of Δ133p53, with consequent modification of p53-mediated transcription, and may modulate the function of p53 in breast and other cancers that harbour wild-type p53.
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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.