ReviewInternational journal of cancer2016
Aberrant splicing of the DMP1-ARF-MDM2-p53 pathway in cancer.
Review in International journal of cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 39 citations in OpenAlex.
- Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization.Molecular oncology · 2026Article
- Prognostic implications of MDM2 expression in surgically resected epidermal growth factor receptor mutant lung cancer with pathological lymph node metastasis.Translational lung cancer research · 2025Article
- MDM2- an indispensable player in tumorigenesis.Molecular biology reports · 2023Review
- How Driver Oncogenes Shape and Are Shaped by Alternative Splicing Mechanisms in Tumors.Cancers · 2023Review
- Antisense Oligonucleotide-Mediated Splice Switching: Potential Therapeutic Approach for Cancer Mitigation.Cancers · 2021Review
- MiR-6838-5p facilitates the proliferation and invasion of renal cell carcinoma cells through inhibiting the DMTF1/ARF-p53 axis.Journal of bioenergetics and biomembranes · 2021Article
- A prognosis-related molecular subtype for early-stage non-small lung cell carcinoma by multi-omics integration analysis.BMC cancer · 2021Article
- Article
- Survival of Lung Cancer Patients Dependent on the LOH Status forInternational journal of molecular sciences · 2020Article
- Post-Translational Regulation of ARF: Perspective in Cancer.Biomolecules · 2020Review
- Review
- c-MYB and DMTF1 in Cancer.Cancer investigation · 2019Review
- Aberrant RNA Splicing in Cancer and Drug Resistance.Cancers · 2018Review
- Translocations involving ETS family proteins in human cancer.Integrative cancer science and therapeutics · 2018Article
- Aberrant expression of p16Cancer reports and reviews · 2018Article
- Alternative Splicing as a Target for Cancer Treatment.International journal of molecular sciences · 2018Review
- Tumor suppression by the EGR1, DMP1, ARF, p53, and PTEN Network.Cancer investigation · 2018Article
- Differential Effects of Autophagy-Related 10 Protein on HCV Replication and Autophagy Flux Are Mediated by Its CysteineFrontiers in immunology · 2018Article
- Aberrant expression of ETS1 and ETS2 proteins in cancer.Cancer reports and reviews · 2018Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Alternative splicing (AS) of mRNA precursors is a ubiquitous mechanism for generating numerous transcripts with different activities from one genomic locus in mammalian cells. The gene products from a single locus can thus have similar, dominant-negative or even opposing functions. Aberrant AS has been found in cancer to express proteins that promote cell growth, local invasion and metastasis. This review will focus on the aberrant splicing of tumor suppressor/oncogenes that belong to the DMP1-ARF-MDM2-p53 pathway. Our recent study shows that the DMP1 locus generates both tumor-suppressive DMP1α (p53-dependent) and oncogenic DMP1β (p53-independent) splice variants, and the DMP1β/α ratio increases with neoplastic transformation of breast epithelial cells. This process is associated with high DMP1β protein expression and shorter survival of breast cancer (BC) patients. Accumulating pieces of evidence show that ARF is frequently inactivated by aberrant splicing in human cancers, demonstrating its involvement in human malignancies. Splice variants from the MDM2 locus promote cell growth in culture and accelerate tumorigenesis in vivo. Human cancers expressing these splice variants are associated with advanced stage/metastasis, and thus have negative clinical impacts. Although they lack most of the p53-binding domain, their activities are mostly dependent on p53 since they bind to wild-type MDM2. The p53 locus produces splice isoforms that have either favorable (β/γ at the C-terminus) or negative impact (Δ40, Δ133 at the N-terminus) on patients' survival. As the oncogenic AS products from these loci are expressed only in cancer cells, they may eventually become targets for molecular therapies.
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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.