ArticleNature communications2020
The RNA-binding protein AKAP8 suppresses tumor metastasis by antagonizing EMT-associated alternative splicing.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 109 citations in OpenAlex.
- Deconvoluting the multi-faceted roles of alternative splicing events in cancer: From underlying mechanisms to innovative therapeutics.Acta pharmaceutica Sinica. B · 2026Review
- Telmisartan Repurposing Targets Novel Biomarkers for Precision Colorectal Cancer Therapy.Pharmaceutics · 2026Article
- TIA1 depletion enhances CLSTN1 exon 11 inclusion to facilitate Epithelial-to-Mesenchymal transition and breast cancer metastasis.Oncogene · 2026Article
- Alternative splicing rewires breast cancer and opens therapeutic avenues.Cell communication and signaling : CCS · 2026Review
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- NXF1 suppresses progression of endometrial cancer by interacting with the SRSF3 to regulate SP4 splicing.iScience · 2025Article
- Strong Signatures of Selection on Candidate Genes Underlying Core Speciation Mechanisms in Desert Tortoises.Molecular ecology resources · 2025Article
- DDX42 Enhances Hepatocellular Carcinoma Cell Proliferation, Radiation and Sorafenib Resistance via Regulating GRB2 RNA Maturation and Activating PI3K/AKT Pathway.Journal of cellular and molecular medicine · 2025Article
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- A Dual Approach with Organoid and CRISPR Screening Reveals ERCC6 as a Determinant of Cisplatin Resistance in Osteosarcoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- GRB2 Promotes Malignant Behaviors of Breast Cancer by Modulating the Global Expression and Alternative Splicing Profiles in SK-BR-3 Cells Through Binding mRNA.Cancer medicine · 2025Article
- HnRNPR-mediated UPF3B mRNA splicing drives hepatocellular carcinoma metastasis.Journal of advanced research · 2025Article
- MAP4 kinase-regulated reduced CLSTN1 expression in medulloblastoma is associated with increased invasiveness.Scientific reports · 2025Article
- Constructing a doxycycline-inducible system for an epithelial-to-mesenchymal transition model in MCF10A cells.Biology open · 2024Article
- Steering research on mRNA splicing in cancer towards clinical translation.Nature reviews. Cancer · 2024Review
- Research progress on the relationship between AURKA and tumorigenesis: the neglected nuclear function of AURKA.Annals of medicine · 2024Review
- Review
- Protein kinase A and local signaling in cancer.The Biochemical journal · 2024Review
- BUB1 induces AKT/mTOR pathway activity to promote EMT induction in human small cell lung cancer.Scientific reports · 2024Article
- Advancements in precision nanomedicine design targeting the anoikis-platelet interface of circulating tumor cells.Acta pharmaceutica Sinica. B · 2024Review
16 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Alternative splicing has been shown to causally contribute to the epithelial-mesenchymal transition (EMT) and tumor metastasis. However, the scope of splicing factors that govern alternative splicing in these processes remains largely unexplored. Here we report the identification of A-Kinase Anchor Protein (AKAP8) as a splicing regulatory factor that impedes EMT and breast cancer metastasis. AKAP8 not only is capable of inhibiting splicing activity of the EMT-promoting splicing regulator hnRNPM through protein-protein interaction, it also directly binds to RNA and alters splicing outcomes. Genome-wide analysis shows that AKAP8 promotes an epithelial cell state splicing program. Experimental manipulation of an AKAP8 splicing target CLSTN1 revealed that splice isoform switching of CLSTN1 is crucial for EMT. Moreover, AKAP8 expression and the alternative splicing of CLSTN1 predict breast cancer patient survival. Together, our work demonstrates the essentiality of RNA metabolism that impinges on metastatic breast cancer.
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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.