ArticleCancers2019
DOCK1 Regulates Growth and Motility through the RRP1B-Claudin-1 Pathway in Claudin-Low Breast Cancer Cells.
Article in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- DOCK1 inhibitor Box5 (TFA) suppresses proliferation of AML cell lines and prolongs survival in AML xenograft models.Scientific reports · 2026Article
- Subtype-Specific mInternational journal of molecular sciences · 2026Article
- Claudins in ovarian cancer: emerging biomarkers and therapeutic targets.Tissue barriers · 2026Review
- Circular RNA microarray expression profile and potential function of circDOCK1 in colorectal cancer.Frontiers in genetics · 2025Article
- Circ_0002669 promotes osteosarcoma tumorigenesis through directly binding to MYCBP and sponging miR-889-3p.Biology direct · 2024Article
- Impact ofCancers · 2024Article
- DOCK1 regulates the malignant biological behavior of endometrial cancer through c-Raf/ERK pathway.BMC cancer · 2024Article
- DOCK1 insufficiency disrupts trophoblast function and pregnancy outcomes via DUSP4-ERK pathway.Life science alliance · 2024Article
- Genome-Wide Association Studies Reveal Candidate Genes Associated with Pigmentation Patterns of Single Feathers of Tianfu Nonghua Ducks.Animals : an open access journal from MDPI · 2023Article
- The Carcinogenic Potential of Bisphenol A in the Liver Based on Transcriptomic Studies.Cancers · 2023Article
- Research progress of Claudin-low breast cancer.Frontiers in oncology · 2023Review
- Article
- Peptide-Based Vaccines in Clinical Phases and New Potential Therapeutic Targets as a New Approach for Breast Cancer: A Review.Vaccines · 2022Review
- Validating RRP12 Expression and Its Prognostic Significance in HCC Based on Data Mining and Bioinformatics Methods.Frontiers in oncology · 2022Article
- Dysregulated expression of claudins in cancer.Oncology letters · 2021Review
- Glucose-limiting conditions induce an invasive population of MDA-MB-231 breast cancer cells with increased connexin 43 expression and membrane localization.Journal of cell communication and signaling · 2021Article
- DNA Hypomethylation of DOCK1 Leading to High Expression Correlates with Neurologic Deterioration and Poor Function Outcomes after Spontaneous Intracerebral Hemorrhage.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Claudin 1 inhibits cell migration and increases intercellular adhesion in triple-negative breast cancer cell line.Molecular biology reports · 2020Article
- RHO to the DOCK for GDP disembarking: Structural insights into the DOCK GTPase nucleotide exchange factors.The Journal of biological chemistryReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dedicator of cytokinesis 1 (DOCK1) is a critical regulator of cancer metastasis. Claudins are transmembrane proteins that play a role in epithelial barrier integrity. Due to a loss or low expression of claudins (CLDN), the claudin-low type of triple-negative breast cancer (TNBC) is characterized by a mesenchymal-like phenotype with strong metastatic potential. In order to elucidate the mechanism of DOCK1 in cancer metastasis, we first analyzed the transcriptomic changes using a clinical database of human TNBC and found that the increase in DOCK1 expression was highly correlated with the poor survival rate of TNBC patients. Interference with DOCK1 expression by shRNA resulted in re-expression of claudin-1 in conjunction with significant inhibition of cell viability and motility of claudin-low breast cancer cells. Accordingly, overexpression of claudin-1 suppressed cell viability and migration. Genetic knockdown and pharmacological blockade of Rac1/Rac2 up-regulated claudin-1. DOCK1 knockdown also caused a decrease in DNA methyltransferase (DNMT) expression and an increase in claudin-1 transcript and promoter activity. Furthermore, RRP1B mediated DOCK1 depletion, which up-regulated claudin-1 expression, cell viability, and motility in claudin-low breast cancer cells. This study demonstrated that DOCK1 mediates growth and motility through down-regulated claudin-1 expression via the RRP1BDNMTclaudin-1 pathway and that claudin-1 serves as an important effector in DOCK1-mediated cancer progression and metastasis in claudin-low breast cancer cells.
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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.