ArticleNature communications2019
Identification of the PTEN-ARID4B-PI3K pathway reveals the dependency on ARID4B by PTEN-deficient prostate cancer.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 53 citations in OpenAlex.
- CDC73 suppresses lung adenocarcinoma via the PTEN/AKT pathway and exhibits biomarker and functional potential in extracellular vesicles.Cell death discovery · 2026Article
- Multi-omics evaluation of cell lines as models for metastatic prostate cancer.Communications biology · 2026Article
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- NAT10-mediated N4-acetylcytidine (ac4C) modification of PIK3R2 mRNA promotes malignant progression of glioblastoma.Cell death & disease · 2025Article
- Review
- ARID4B Promotes the Progression of Hepatocellular Carcinoma Through the PI3K/AKT Pathway.Annals of surgical oncology · 2025Article
- Machine learning selection of basement membrane-associated genes and development of a predictive model for kidney fibrosis.Scientific reports · 2025Article
- Current trends in sensitizing immune checkpoint inhibitors for cancer treatment.Molecular cancer · 2024Review
- Targeting mRNA-coding genes in prostate cancer using CRISPR/Cas9 technology with a special focus on androgen receptor signaling.Cell communication and signaling : CCS · 2024Review
- Adipose-Derived Stem-Cell-Membrane-Coated PLGA-PEI Nanoparticles Promote Wound Healing via Efficient Delivery of miR-21.Pharmaceutics · 2024Article
- Exosomes: compositions, biogenesis, and mechanisms in diabetic wound healing.Journal of nanobiotechnology · 2024Review
- Heterozygous Knockout ofGenes · 2023Article
- ARID3a from the ARID family: structure, role in autoimmune diseases and drug discovery.Acta pharmacologica Sinica · 2023Review
- CRISPR-Cas9 Library Screening Identifies Novel Molecular Vulnerabilities inInternational journal of molecular sciences · 2023Article
- BRF2 is mediated by microRNA-409-3p and promotes invasion and metastasis of HCC through the Wnt/β-catenin pathway.Cancer cell international · 2023Article
- Aberrant PI3Kδ splice isoform as a potential biomarker and novel therapeutic target for endocrine cancers.Frontiers in endocrinology · 2023Article
- Isobavachalcone's Alleviation of Pyroptosis Contributes to Enhanced Apoptosis in Glioblastoma: Possible Involvement of NLRP3.Molecular neurobiology · 2022Article
- Comprehensive characterization of posttranscriptional impairment-related 3'-UTR mutations in 2413 whole genomes of cancer patients.NPJ genomic medicine · 2022Article
- Missense Variants Reveal Functional Insights Into the Human ARID Family of Gene Regulators.Journal of molecular biology · 2022Article
- Positive Selection and Enhancer Evolution Shaped Lifespan and Body Mass in Great Apes.Molecular biology and evolution · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
PTEN is frequently mutated in prostate cancer. The tumor suppressor function of PTEN is attributed to its lipid phosphatase activity that counters PI3K action. Here, we report a PTEN-ARID4B-PI3K axis in which PTEN inhibits expression of ARID4B, while ARID4B is a transcriptional activator of the PI3K subunit genes PIK3CA and PIK3R2 that are crucial for activation of the PI3K/AKT pathway. Reciprocal binding of ARID4B and histone H1 to the PIK3CA and PIK3R2 promoters modulates chromatin condensation, suggesting a mechanism by which ARID4B activates these promoters. Functional analyses reveals that ARID4B is required for prostate tumorigenesis when PTEN is deficient. The biological significance is further substantiated by the existence of a PTEN/ARID4B/PIK3CA three-gene signature that improves the predictive power for prostate cancer recurrence in patients. In summary, we identify ARID4B as a master regulator in the PTEN-PI3K pathway, thus providing a potential therapeutic target for prostate cancer carrying PTEN mutations.
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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.