ArticlePloS one2012
Tetraspanin CD82 inhibits protrusion and retraction in cell movement by attenuating the plasma membrane-dependent actin organization.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
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Who cites it
23 citing papers in PubMed, 44 citations in OpenAlex.
- Interaction between CD82 and integrin αVβ3 selectively regulates collective movement of tumor cells via endolysosomal trafficking.Cellular and molecular life sciences : CMLS · 2026Article
- Network analysis of gene expression reveals regulators of cell viscosity and mechanical phenotype.Scientific reports · 2025Article
- Evaluating the effects of various ethanolic medicinal plant extracts on metastatic breast cancer proliferation, invasion, and expression of a novel potential drug target; CD82 metastatic suppressor protein, and on in vivo angiogenesis using the ex ovo yolk sac membrane (YSM) assay.Journal of cancer research and clinical oncology · 2024Article
- Article
- KAI1(CD82) is a key molecule to control angiogenesis and switch angiogenic milieu to quiescent state.Journal of hematology & oncology · 2021Article
- Targeting CD82/KAI1 for Precision Therapeutics in Surmounting Metastatic Potential in Breast Cancer.Cancers · 2021Review
- Mechanical Control of Cell Migration by the Metastasis Suppressor Tetraspanin CD82/KAI1.Cells · 2021Article
- Tetraspanin CD82 interaction with cholesterol promotes extracellular vesicle-mediated release of ezrin to inhibit tumour cell movement.Journal of extracellular vesicles · 2020Article
- CD82 controls CpG-dependent TLR9 signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Regulation of cytoskeleton and adhesion signaling in osteoclasts by tetraspanin CD82.Bone reports · 2019Article
- Clinical significance of MACC1, Twist1, and KAI1 expressions in infiltrating urothelial carcinoma of the bladder.International journal of clinical and experimental pathology · 2019Article
- The tetraspanin CD82 regulates bone marrow homing and engraftment of hematopoietic stem and progenitor cells.Molecular biology of the cell · 2018Article
- Tetraspanin-enriched microdomains regulate digitation junctions.Cellular and molecular life sciences : CMLS · 2018Article
- Associations of MACC1, AGR2, and KAI1 expression with the metastasis and prognosis in head and neck squamous cell carcinoma.International journal of clinical and experimental pathology · 2018Article
- Tetraspanins, Another Piece in the HIV-1 Replication Puzzle.Frontiers in immunology · 2018Review
- The cancer-associated cell migration protein TSPAN1 is under control of androgens and its upregulation increases prostate cancer cell migration.Scientific reports · 2017Article
- Tetraspanins Function as Regulators of Cellular Signaling.Frontiers in cell and developmental biology · 2017Review
- The expression of metastasis-associated in colon cancer-1 and KAI1 in gastric adenocarcinoma and their clinical significance.World journal of surgical oncology · 2016Article
- Function and Dynamics of Tetraspanins during Antigen Recognition and Immunological Synapse Formation.Frontiers in immunology · 2015Review
- Tetraspanins in cell migration.Cell adhesion & migration · 2015Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
To determine how tetraspanin KAI1/CD82, a tumor metastasis suppressor, inhibits cell migration, we assessed which cellular events critical for motility are altered by KAI1/CD82 and how KAI1/CD82 regulates these events. We found that KAI1/CD82-expressing cells typically exhibited elongated cellular tails and diminished lamellipodia. Live imaging demonstrated that the polarized protrusion and retraction of the plasma membrane became deficient upon KAI1/CD82 expression. The deficiency in developing these motility-related cellular events was caused by poor formations of actin cortical network and stress fiber and by aberrant dynamics in actin organization. Rac1 activity was reduced by KAI1/CD82, consistent with the diminution of lamellipodia and actin cortical network; while the growth factor-stimulated RhoA activity was blocked by KAI1/CD82, consistent with the loss of stress fiber and attenuation in cellular retraction. Upon KAI1/CD82 expression, Rac effector cofilin was not enriched at the cell periphery to facilitate lamellipodia formation while Rho kinase exhibited a significantly lower activity leading to less retraction. Phosphatidylinositol 4, 5-biphosphate, which initiates actin polymerization from the plasma membrane, became less detectable at the cell periphery in KAI1/CD82-expressing cells. Moreover, KAI1/CD82-induced phenotypes likely resulted from the suppression of multiple signaling pathways such as integrin and growth factor signaling. In summary, at the cellular level KAI1/CD82 inhibited polarized protrusion and retraction events by disrupting actin reorganization; at the molecular level, KAI1/CD82 deregulated Rac1, RhoA, and their effectors cofilin and Rho kinase by perturbing the plasma membrane lipids.
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What OpenQuestion holds
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.