ArticlePLoS genetics2011
An EMT-driven alternative splicing program occurs in human breast cancer and modulates cellular phenotype.
Article in PLoS genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03694756 (TMEM-MRI), which is not on this map. Cited by 307 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.
TMEM-MRI: A Pilot Feasibility Study of Magnetic Resonance Imaging for Imaging of TMEM (Tumor Microenvironment of Metastasis) in Patients With Operable Breast Cancer
Who cites it
307 citing papers in PubMed, 19 citations in OpenAlex.
- Immune-associated alternative splicing signatures define molecular subtypes in breast cancer.iScience · 2026Article
- The RNA-binding protein RBFOX2 suppresses colorectal cancer proliferation and metastasis by reducing FUBP1 mRNA stability to induce mitochondrial dysfunction and ferroptosis.Discover oncology · 2026Article
- Forces that shape the transcriptome: Linking cellular mechanosensing to mRNA splicing.The Journal of biological chemistry · 2026Review
- ESRP1 drives epithelial-mesenchymal transition by activating EPAC-RAP1A signaling axis.Frontiers in medicine · 2026Article
- Splice Isoforms of the Apoptosis Gene BCL-X Have Opposing Effects in Diabetic Kidney Disease: Potential Treatment Target and Prognostic Value.Journal of diabetes research · 2026Article
- APDCA: An accurate and effective method for predicting associations between RBPs and AS-events during epithelial-mesenchymal transition.PLoS computational biology · 2025Article
- PRMT5 regulates alternative splicing of TCF3 under hypoxia to promote EMT and invasion in breast cancer.PLoS biology · 2025Article
- ESRP1 exerts anti-tumor role by promoting ferroptosis in diffuse-type gastric cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- Review
- Global profiling of alternative splicing in non-small cell lung cancer reveals novel histological and population differences.Oncogene · 2025Article
- The Rbfox1/LASR complex controls alternative pre-mRNA splicing by recognition of multipart RNA regulatory modules.Genes & development · 2025Article
- Best evidence linking the extracellular factor TGF-β to cancer-associated alternative splicing programs.BBA advances · 2025Review
- The role of ESRP1 in solid tumor development through the regulation of CD44 splicing and EMT processes.Frontiers in oncology · 2025Review
- SEMA6A overexpression inhibited tumor growth and metastasis in colorectal cancer.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025Article
- Down-regulation of ESRP2 inhibits breast cancer cell proliferation via inhibiting cyclinD1.Scientific reports · 2024Article
- Article
- Functional analysis of ESRP1/2 gene variants and CTNND1 isoforms in orofacial cleft pathogenesis.Communications biology · 2024Article
- Functional analysis ofbioRxiv : the preprint server for biology · 2024Article
- Guardians and Mediators of Metastasis: Exploring T Lymphocytes, Myeloid-Derived Suppressor Cells, and Tumor-Associated Macrophages in the Breast Cancer Microenvironment.International journal of molecular sciences · 2024Review
- Quantitative estimates of the regulatory influence of long non-coding RNAs on global gene expression variation using TCGA breast cancer transcriptomic data.PLoS computational biology · 2024Article
247 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Epithelial-mesenchymal transition (EMT), a mechanism important for embryonic development, plays a critical role during malignant transformation. While much is known about transcriptional regulation of EMT, alternative splicing of several genes has also been correlated with EMT progression, but the extent of splicing changes and their contributions to the morphological conversion accompanying EMT have not been investigated comprehensively. Using an established cell culture model and RNA-Seq analyses, we determined an alternative splicing signature for EMT. Genes encoding key drivers of EMT-dependent changes in cell phenotype, such as actin cytoskeleton remodeling, regulation of cell-cell junction formation, and regulation of cell migration, were enriched among EMT-associated alternatively splicing events. Our analysis suggested that most EMT-associated alternative splicing events are regulated by one or more members of the RBFOX, MBNL, CELF, hnRNP, or ESRP classes of splicing factors. The EMT alternative splicing signature was confirmed in human breast cancer cell lines, which could be classified into basal and luminal subtypes based exclusively on their EMT-associated splicing pattern. Expression of EMT-associated alternative mRNA transcripts was also observed in primary breast cancer samples, indicating that EMT-dependent splicing changes occur commonly in human tumors. The functional significance of EMT-associated alternative splicing was tested by expression of the epithelial-specific splicing factor ESRP1 or by depletion of RBFOX2 in mesenchymal cells, both of which elicited significant changes in cell morphology and motility towards an epithelial phenotype, suggesting that splicing regulation alone can drive critical aspects of EMT-associated phenotypic changes. The molecular description obtained here may aid in the development of new diagnostic and prognostic markers for analysis of breast cancer progression.
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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.