ArticleThe Journal of biological chemistry2011
mda-9/Syntenin protein positively regulates the activation of Akt protein by facilitating integrin-linked kinase adaptor function during adhesion to type I collagen.
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 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- MDA-9/Syntenin as a therapeutic cancer metastasis target: current molecular and preclinical understanding.Expert opinion on therapeutic targets · 2025Review
- The Multifunctional Protein Syntenin-1: Regulator of Exosome Biogenesis, Cellular Function, and Tumor Progression.International journal of molecular sciences · 2023Review
- Biological Role and Aberrant Overexpression of Syntenin-1 in Cancer: Potential Role as a Biomarker and Therapeutic Target.Biomedicines · 2023Review
- Targeting the two-pore channel 2 in cancer progression and metastasis.Exploration of targeted anti-tumor therapy · 2022Review
- Prune-1 drives polarization of tumor-associated macrophages (TAMs) within the lung metastatic niche in triple-negative breast cancer.iScience · 2021Article
- The role of collagen in cancer: from bench to bedside.Journal of translational medicine · 2019Review
- Effects of syndecan-1 on the expression of syntenin and the migration of U251 glioma cells.Oncology letters · 2017Article
- Inhibition of radiation-induced glioblastoma invasion by genetic and pharmacological targeting of MDA-9/Syntenin.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
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- Knockout of MDA-9/Syntenin (SDCBP) expression in the microenvironment dampens tumor-supporting inflammation and inhibits melanoma metastasis.Oncotarget · 2016Article
- Examination of Epigenetic and other Molecular Factors Associated with mda-9/Syntenin Dysregulation in Cancer Through Integrated Analyses of Public Genomic Datasets.Advances in cancer research · 2015Review
- Targeting tumor invasion: the roles of MDA-9/Syntenin.Expert opinion on therapeutic targets · 2015Review
- Novel role of MDA-9/syntenin in regulating urothelial cell proliferation by modulating EGFR signaling.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013Article
- Elevated expression of syntenin in breast cancer is correlated with lymph node metastasis and poor patient survival.Breast cancer research : BCR · 2013Article
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- Binding to syntenin-1 protein defines a new mode of ubiquitin-based interactions regulated by phosphorylation.The Journal of biological chemistry · 2011Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The integrin-linked kinase (ILK)-PINCH1-α-parvin (IPP) complex functions as a signaling platform for integrins that modulates various cellular processes. ILK functions as a central adaptor for the assembly of IPP complex. We report here that mda-9/syntenin, a positive regulator of cancer metastasis, regulates the activation of Akt (also known as protein kinase B) by facilitating ILK adaptor function during adhesion to type I collagen (COL-I) in human breast cancer cells. COL-I stimulation induced the phosphorylation and plasma membrane translocation of Akt. Inhibition of mda-9/syntenin or expression of mutant ILK (E359K) significantly blocked the translocation of both ILK and Akt to the plasma membrane. mda-9/syntenin associated with ILK, and this association was increased at the plasma membrane by COL-I stimulation. Knockdown of mda-9/syntenin impaired COL-I-induced association of ILK with Akt and plasma membrane targeting of ILK-Akt complex. These results demonstrated that mda-9/syntenin regulates the activation of Akt by controlling the plasma membrane targeting of Akt via a mechanism that facilitates the association of Akt with ILK at the plasma membrane during adhesion to COL-I. On a striking note, inhibition of mda-9/syntenin impaired COL-I-induced plasma membrane translocation of the IPP complex and assembly of integrin β1-IPP signaling complexes. Thus, our study defines the role of mda-9/syntenin in ILK adaptor function and describes a new mechanism of mda-9/syntenin for regulation of cell migration.
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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.