ReviewAmerican journal of cancer research2021
MDM4 alternative splicing and implication in MDM4 targeted cancer therapies.
Review in American journal of cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 18 citations in OpenAlex.
- From COPD and asthma to lung cancer: potential candidate genes and their associated biological pathways for the incidence risk of lung cancer.Journal, genetic engineering & biotechnology · 2026Article
- Pharmacological targeting of SF3a1-MDM4 splicing vulnerability in ovarian cancer with rifaximin and antisense oligonucleotide.Journal of translational medicine · 2026Article
- New evidence for the protective effect of gut microbiota regulation of ferroptosis-related proteins against osteoporosis.World journal of microbiology & biotechnology · 2025Article
- NS3 of hepatitis C virus drives hepatocellular carcinoma progression through a novel RNA-interference pathway.Journal of cell communication and signaling · 2025Article
- Article
- Structure and function of MDM2 and MDM4 in health and disease.The Biochemical journal · 2025Review
- SNRPB2 promotes triple-negative breast cancer progression by controlling alternative splicing of MDM4 pre-mRNA.Cancer science · 2024Article
- A defective splicing machinery promotes senescence through MDM4 alternative splicing.Aging cell · 2024Article
- SETBP1 activation upon MDM4-enhanced ubiquitination of NR3C1 triggers dissemination of colorectal cancer cells.Clinical & experimental metastasis · 2024Article
- LINC01094: A key long non-coding RNA in the regulation of cancer progression and therapeutic targets.Heliyon · 2024Review
- Long-Read MDM4 Sequencing Reveals Aberrant Isoform Landscape in Metastatic Melanomas.International journal of molecular sciences · 2024Article
- Multi-tissue transcriptome-wide association studies identified 235 genes for intrinsic subtypes of breast cancer.Journal of the National Cancer Institute · 2024Article
- Regulation of p53 by the mitotic surveillance/stopwatch pathway: implications in neurodevelopment and cancer.Frontiers in cell and developmental biology · 2024Review
- The nuclear GYF protein CD2BP2/U5-52K is required for T cell homeostasis.Frontiers in immunology · 2024Article
- Recent findings on miR‑370 expression, regulation and functions in cancer (Review).Oncology reports · 2023Review
- Targeting MDM4 as a Novel Therapeutic Approach in Prostate Cancer Independent of p53 Status.Cancers · 2022Article
- Review
- Identification of EMT-related alternative splicing event of TMC7 to promote invasion and migration of pancreatic cancer.Frontiers in immunology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
The oncogenic MDM4, initially named MDMX, has been identified as a p53-interacting protein and a key upstream negative regulator of the tumor suppressor p53. Accumulating evidence indicates that MDM4 plays critical roles in the initiation and progression of multiple human cancers. MDM4 is frequently amplified and upregulated in human cancers, contributing to overgrowth and apoptosis inhibition by blocking the expression of downstream target genes of p53 pathway. Disruptors for MDM4-p53 interaction have been shown to restore the anti-tumor activity of p53 in cancer cells. MDM4 possesses multiple splicing isoforms whose expressions are driven by the presence of oncogenes in cancer cells. Some of the MDM4 splicing isoforms lack p53 binding domain and may exhibit p53-independent oncogenic functions. These features render MDM4 to be an attractive therapeutic target for cancer therapy. In the present review, we primarily focus on the detailed molecular structure of MDM4 splicing isoforms, candidate regulators for initiating MDM4 splicing, deregulation of MDM4 isoforms in cancer and potential therapy strategies by targeting splicing isoforms of MDM4.
Indexed as
Identifiers
35018230PMC8727814W4206872300What OpenQuestion holds
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.