ArticleThe Journal of biological chemistry2011
Rap1-GTP-interacting adaptor molecule (RIAM) protein controls invasion and growth of melanoma cells.
Article in The Journal of biological chemistry, 2011. 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, 40 citations in OpenAlex.
- Adaptor proteins regulating tumor-associated macrophage polarization during cancer progression.Oncoscience · 2026Review
- IgSF11-RAP1 signaling promotes cell migration and invasion of cutaneous melanoma.Cell communication and signaling : CCS · 2025Article
- Ras-proximate-1 (RAP1): a prognosis and therapeutic target in the metastatic spread of breast cancer.Clinical & experimental metastasis · 2025Review
- Potential predictive value of circulating tumor DNA (ctDNA) mutations for the efficacy of immune checkpoint inhibitors in advanced triple-negative breast cancer.Frontiers in genetics · 2023Article
- Expression of the phagocytic receptors αFrontiers in immunology · 2022Article
- Development and validation of prognostic markers in sarcomas base on a multi-omics analysis.BMC medical genomics · 2021Article
- Immunological Role and Prognostic Value of APBB1IP in Pan-Cancer Analysis.Journal of Cancer · 2021Article
- Subversion of Ras Small GTPases in Cutaneous Melanoma Aggressiveness.Frontiers in cell and developmental biology · 2020Review
- miR-204-5p and miR-211-5p Contribute to BRAF Inhibitor Resistance in Melanoma.Cancer research · 2018Article
- Roles of Rap1 signaling in tumor cell migration and invasion.Cancer biology & medicine · 2017Article
- Article
- Nuclear SIPA1 activates integrin β1 promoter and promotes invasion of breast cancer cells.Oncogene · 2015Article
- Article
- Glucocorticoids mediate induction of microRNA-708 to suppress ovarian cancer metastasis through targeting Rap1B.Nature communications · 2015Article
- Conformational activation of talin by RIAM triggers integrin-mediated cell adhesion.Nature communications · 2014Article
- The on-off relationship of Rho and Rac during integrin-mediated adhesion and cell migration.Small GTPases · 2014Review
- Phosphorylation-mediated regulation of GEFs for RhoA.Cell adhesion & migration · 2014Review
- Insights into TREM2 biology by network analysis of human brain gene expression data.Neurobiology of aging · 2013Article
- Protein kinase A-dependent phosphorylation of Rap1 regulates its membrane localization and cell migration.The Journal of biological chemistry · 2013Article
- RIAM (Rap1-interacting adaptor molecule) regulates complement-dependent phagocytosis.Cellular and molecular life sciences : CMLS · 2013Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 3 countries.
Funding
Abstract
The Mig-10/RIAM/lamellipodin (MRL) family member Rap1-GTP-interacting adaptor molecule (RIAM) interacts with active Rap1, a small GTPase that is frequently activated in tumors such as melanoma and prostate cancer. We show here that RIAM is expressed in metastatic human melanoma cells and that both RIAM and Rap1 are required for BLM melanoma cell invasion. RIAM silencing in melanoma cells led to inhibition of tumor growth and to delayed metastasis in a severe combined immunodeficiency xenograft model. Defective invasion of RIAM-silenced melanoma cells arose from impairment in persistent cell migration directionality, which was associated with deficient activation of a Vav2-RhoA-ROCK-myosin light chain pathway. Expression of constitutively active Vav2 and RhoA in cells depleted for RIAM partially rescued their invasion, indicating that Vav2 and RhoA mediate RIAM function. These results suggest that inhibition of cell invasion in RIAM-silenced melanoma cells is likely based on altered cell contractility and cell polarization. Furthermore, we show that RIAM depletion reduces β1 integrin-dependent melanoma cell adhesion, which correlates with decreased activation of both Erk1/2 MAPK and phosphatidylinositol 3-kinase, two central molecules controlling cell growth and cell survival. In addition to causing inhibition of cell proliferation, RIAM silencing led to higher susceptibility to cell apoptosis. Together, these data suggest that defective activation of these kinases in RIAM-silenced cells could account for inhibition of melanoma cell growth and that RIAM might contribute to the dissemination of melanoma cells.
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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.