ArticleOncogene2006
Tetraspanin KAI1/CD82 suppresses invasion by inhibiting integrin-dependent crosstalk with c-Met receptor and Src kinases.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
What it found
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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
70 citing papers in PubMed, 155 citations in OpenAlex.
- ITGA3-MET interaction promotes papillary thyroid cancer progression via ERK and PI3K/AKT pathways.Annals of medicine · 2025Article
- The MET Oncogene Network of Interacting Cell Surface Proteins.International journal of molecular sciences · 2024Review
- A peptide interfering with the dimerization of oncogenic KITENIN protein and its stability suppresses colorectal tumour progression.Clinical and translational medicine · 2022Article
- CD82 palmitoylation site mutations at Cys5+Cys74 affect EGFR internalization and metabolism through recycling pathway.Acta biochimica et biophysica Sinica · 2022Article
- c-Met-integrin cooperation: Mechanisms, tumorigenic effects, and therapeutic relevance.Frontiers in cell and developmental biology · 2022Review
- Tetraspanins: Physiology, Colorectal Cancer Development, and Nanomediated Applications.Cancers · 2021Review
- Role of a metastatic suppressor gene KAI1/CD82 in the diagnosis and prognosis of breast cancer.Saudi journal of biological sciences · 2021Review
- Gene expression analysis of human prostate cell lines with and without tumor metastasis suppressor CD82.BMC cancer · 2020Article
- Tetraspanin CD82 is necessary for muscle stem cell activation and supports dystrophic muscle function.Skeletal muscle · 2020Article
- CMTM5-v1 inhibits cell proliferation and migration by downregulating oncogenic EGFR signaling in prostate cancer cells.Journal of Cancer · 2020Article
- Extracellular Matrix-Associated Factors Play Critical Roles in Regulating Pancreatic β-Cell Proliferation and Survival.Endocrinology · 2019Review
- Transcriptome Analysis of Yamame (Biology · 2019Article
- KAI1/CD82 Genetically Engineered Endothelial Progenitor Cells Inhibit Metastasis of Human Nasopharyngeal Carcinoma in a Mouse Model.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Differential tumor biological role of the tumor suppressor KAI1 and its splice variant in human breast cancer cells.Oncotarget · 2018Article
- A viral microRNA downregulates metastasis suppressor CD82 and induces cell invasion and angiogenesis by activating the c-Met signaling.Oncogene · 2017Article
- Tetraspanins Function as Regulators of Cellular Signaling.Frontiers in cell and developmental biology · 2017Review
- CD82 suppresses CD44 alternative splicing-dependent melanoma metastasis by mediating U2AF2 ubiquitination and degradation.Oncogene · 2016Article
- Receptor tyrosine kinase Met promotes cell survival via kinase-independent maintenance of integrin α3β1.Molecular biology of the cell · 2016Article
- Pancreatic cancer stem cell markers and exosomes - the incentive push.World journal of gastroenterology · 2016Review
- TM4SF1 Promotes Proliferation, Invasion, and Metastasis in Human Liver Cancer Cells.International journal of molecular sciences · 2016Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
KAI1/CD82, a tetraspanin protein, was first identified as a metastasis suppressor in prostate cancer. How loss of CD82 expression promotes cancer metastasis is unknown. Restoration of CD82 expression to physiological levels in the metastatic prostate cell line PC3 inhibits integrin-mediated cell migration and invasion, but does not affect integrin expression. Integrin-dependent activation of the receptor kinase c-Met is dramatically reduced in CD82-expressing cells, as is c-Met activation by its ligand HGF/SF. CD82 expression also reduced integrin-induced activation and phosphorylation of the cytoplasmic tyrosine kinase Src, and its downstream substrates p130Cas and FAK Y861. Inhibition of c-Met expression or Src kinase function reduced matrigel invasion of PC3 cells to the same extent as CD82 expression. These data indicate that CD82 functions to suppress integrin-induced invasion by regulating signaling to c-Met and Src kinases, and suggests that CD82 loss may promote metastasis by removing a negative regulator of c-Met and Src signaling.
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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.