ArticleNeoplasia (New York, N.Y.)2018
Downregulation of Rap1Gap: A Switch from DCIS to Invasive Breast Carcinoma via ERK/MAPK Activation.
Article in Neoplasia (New York, N.Y.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
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- Network-based exploration of 4-(phenylsulfonyl)morpholine molecules for metastatic triple-negative breast cancer suppression.PLoS computational biology · 2026Article
- MAZ-Mediated ubiquitin-conjugating enzyme E2C upregulation promotes breast cancer progression via the MAPK signaling pathway.Translational oncology · 2026Article
- PathCLAST: pathway-augmented contrastive learning with attention for interpretable spatial transcriptomics.Briefings in bioinformatics · 2026Article
- Particulate Matter 2.5 Induces FGFR1-mediated Integrin Switch to Promote Non-small Cell Lung Cancer Metastasis.Cancer genomics & proteomics · 2025Article
- Review
- Chaihu Longgu Muli Decoction inhibits chronic stress-induced lung cancer epithelial-mesenchymal transition process by suppressing Rap1/ERK signal pathway.Frontiers in pharmacology · 2025Article
- Magnetic Carbon Bead-Based Concentration Method for SARS-CoV-2 Detection in Wastewater.Food and environmental virology · 2024Article
- Cordycepin Triphosphate as a Potential Modulator of Cellular Plasticity in Cancer via cAMP-Dependent Pathways: An In Silico Approach.International journal of molecular sciences · 2024Article
- SGLT1 as an adverse prognostic factor in invasive ductal carcinoma of the breast.Breast cancer research and treatment · 2023Article
- Chromosome-level Asian elephant genome assembly and comparative genomics of long-lived mammals reveal the common substitutions for cancer resistance.Aging cell · 2023Article
- Epigenetic regulation of LINC01270 in breast cancer progression by mediating LAMA2 promoter methylation and MAPK signaling pathway.Cell biology and toxicology · 2023Article
- Evaluation ofAdvanced biomedical research · 2023Article
- Ductal Carcinoma In Situ of Breast: From Molecular Etiology to Therapeutic Management.Endocrinology · 2022Review
- Transcriptomic Properties of HER2+ Ductal Carcinoma In Situ of the Breast Associate with Absence of Immune Cells.Biology · 2021Article
- Silencing of Nek2 suppresses the proliferation, migration and invasion and induces apoptosis of breast cancer cells by regulating ERK/MAPK signaling.Journal of molecular histology · 2021Article
- Mex3a promotes oncogenesis through the RAP1/MAPK signaling pathway in colorectal cancer and is inhibited by hsa-miR-6887-3p.Cancer communications (London, England) · 2021Article
- Sprouty4 negatively regulates ERK/MAPK signaling and the transition from in situ to invasive breast ductal carcinoma.PloS one · 2021Article
- Analysis of key genes and pathways in breast ductal carcinomaOncology letters · 2020Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Diagnosis of breast ductal carcinoma in situ (DCIS) presents a challenge since we cannot yet distinguish those cases that would remain indolent and not require aggressive treatment from cases that may progress to invasive ductal cancer (IDC). The purpose of this study is to determine the role of Rap1Gap, a GTPase activating protein, in the progression from DCIS to IDC. Immunohistochemistry (IHC) analysis of samples from breast cancer patients shows an increase in Rap1Gap expression in DCIS compared to normal breast tissue and IDCs. In order to study the mechanisms of malignant progression, we employed an in vitro three-dimensional (3D) model that more accurately recapitulates both structural and functional cues of breast tissue. Immunoblotting results show that Rap1Gap levels in MCF10.Ca1D cells (a model of invasive carcinoma) are reduced compared to those in MCF10.DCIS (a model of DCIS). Retroviral silencing of Rap1Gap in MCF10.DCIS cells activated extracellular regulated kinase (ERK) mitogen-activated protein kinase (MAPK), induced extensive cytoskeletal reorganization and acquisition of mesenchymal phenotype, and enhanced invasion. Enforced reexpression of Rap1Gap in MCF10.DCIS-Rap1GapshRNA cells reduced Rap1 activity and reversed the mesenchymal phenotype. Similarly, introduction of dominant negative Rap1A mutant (Rap1A-N17) in DCIS-Rap1Gap shRNA cells caused a reversion to nonmalignant phenotype. Conversely, expression of constitutively active Rap1A mutant (Rap1A-V12) in noninvasive MCF10.DCIS cells led to phenotypic changes that were reminiscent of Rap1Gap knockdown. Thus, reduction of Rap1Gap in DCIS is a potential switch for progression to an invasive phenotype. The Graphical Abstract summarizes these findings.
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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.