ArticleNAR cancer2020
Hypoxia-induced TGF-β-RBFOX2-ESRP1 axis regulates human MENA alternative splicing and promotes EMT in breast cancer.
Article in NAR cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
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
34 citing papers in PubMed, 53 citations in OpenAlex.
- Identifying breast cancer subtypes and exploring spatial expression patterns of the key subtype-specific gene based on pathological images, single-cell sequencing, and spatial transcriptomic data.Breast cancer (Tokyo, Japan) · 2026Article
- Reciprocal regulation of hMENA and TGF-β signaling in cancer-associated fibroblasts promotes EMT, immunosuppression, poor prognosis, and ICT resistance in NSCLC.Journal for immunotherapy of cancer · 2026Article
- ESRP1 drives epithelial-mesenchymal transition by activating EPAC-RAP1A signaling axis.Frontiers in medicine · 2026Article
- PRMT5 regulates alternative splicing of TCF3 under hypoxia to promote EMT and invasion in breast cancer.PLoS biology · 2025Article
- USP9X integrates TGF-β and hypoxia signalings to promote ovarian cancer chemoresistance via HIF-2α-maintained stemness.Cell death & disease · 2025Article
- Hypoxia-induced ATF3 escalates breast cancer invasion by increasing collagen deposition via P4HA1.Cell death & disease · 2025Article
- The role of ESRP1 in solid tumor development through the regulation of CD44 splicing and EMT processes.Frontiers in oncology · 2025Review
- The splicing machinery is dysregulated and represents a therapeutic vulnerability in breast cancer.Cellular and molecular life sciences : CMLS · 2024Article
- Article
- Upregulation of ENAH by a PI3K/AKT/β-catenin cascade promotes oral cancer cell migration and growth via an ITGB5/Src axis.Cellular & molecular biology letters · 2024Article
- Article
- RNA splicing factor RBFOX2 is a key factor in the progression of cancer and cardiomyopathy.Clinical and translational medicine · 2024Review
- Review
- RBFOX2 deregulation promotes pancreatic cancer progression and metastasis through alternative splicing.Nature communications · 2023Article
- Role of epithelial splicing regulatory protein 1 in cancer progression.Cancer cell international · 2023Review
- Review
- Small extracellular vesicle TGF-β in cancer progression and immune evasion.Cancer gene therapy · 2023Review
- PKM2 dictates the poised chromatin state ofNAR cancer · 2023Article
- The discovery, function, and regulation of epithelial splicing regulatory proteins (ESRP) 1 and 2.Biochemical Society transactions · 2023Article
- Hypoxia-induced loss of SRSF2-dependent DNA methylation promotes CTCF-mediated alternative splicing of VEGFA in breast cancer.iScience · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Hypoxic microenvironment heralds epithelial-mesenchymal transition (EMT), invasion and metastasis in solid tumors. Deregulation of alternative splicing (AS) of several cancer-associated genes has been instrumental in hypoxia-induced EMT. Our study in breast cancer unveils a previously unreported mechanism underlying hypoxia-mediated AS of
Identifiers
What 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.