ArticleThe American journal of pathology2009
Transmembrane interactions are needed for KAI1/CD82-mediated suppression of cancer invasion and metastasis.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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
32 citing papers in PubMed, 52 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
- The neuroscience of cancer: Focus on neuropeptidergic systems.Acta pharmaceutica Sinica. B · 2025Review
- Article
- Molecular interaction of metastasis suppressor genes and tumor microenvironment in breast cancer.Exploration of targeted anti-tumor therapy · 2023Review
- Decreased TSPAN14 Expression Contributes to NSCLC Progression.Life (Basel, Switzerland) · 2022Article
- Liprins in oncogenic signaling and cancer cell adhesion.Oncogene · 2021Review
- Targeting CD82/KAI1 for Precision Therapeutics in Surmounting Metastatic Potential in Breast Cancer.Cancers · 2021Review
- Tetraspanin CD82 is necessary for muscle stem cell activation and supports dystrophic muscle function.Skeletal muscle · 2020Article
- Investigations of a Possible Role of SNPs in KAI1 Gene on Its Down-Regulation in Breast Cancer.Asian Pacific journal of cancer prevention : APJCP · 2020Article
- Melanoblast transcriptome analysis reveals pathways promoting melanoma metastasis.Nature communications · 2020Article
- Tetraspanin CD82 interaction with cholesterol promotes extracellular vesicle-mediated release of ezrin to inhibit tumour cell movement.Journal of extracellular vesicles · 2020Article
- Liprin-α1 modulates cancer cell signaling by transmembrane protein CD82 in adhesive membrane domains linked to cytoskeleton.Cell communication and signaling : CCS · 2018Article
- A survey of metastasis suppressors in Metazoa.Laboratory investigation; a journal of technical methods and pathology · 2018Review
- Differential tumor biological role of the tumor suppressor KAI1 and its splice variant in human breast cancer cells.Oncotarget · 2018Article
- Kisspeptin and Cancer: Molecular Interaction, Biological Functions, and Future Perspectives.Frontiers in endocrinology · 2018Review
- A viral microRNA downregulates metastasis suppressor CD82 and induces cell invasion and angiogenesis by activating the c-Met signaling.Oncogene · 2017Article
- Tspan2: a tetraspanin protein involved in oligodendrogenesis and cancer metastasis.Biochemical Society transactions · 2017Review
- Nm23-H1 was involved in regulation of KAI1 expression in high-metastatic lung cancer cells L9981.Journal of thoracic disease · 2016Article
- Tetraspanins in cell migration.Cell adhesion & migration · 2015Review
- Regulation of FAK Activity by Tetraspan Proteins: Potential Clinical Implications in Cancer.Critical reviews in oncogenesis · 2015Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
In transmembrane (TM) domains, tetraspanin KAI1/CD82 contains an Asn, a Gln, and a Glu polar residue. A mutation of all three polar residues largely disrupts the migration-, invasion-, and metastasis-suppressive activities of KAI1/CD82. Notably, KAI1/CD82 inhibits the formation of microprotrusions and the release of microvesicles, while the mutation disrupts these inhibitions, revealing the connections of microprotrusion and microvesicle to KAI1/CD82 function. The TM polar residues are needed for proper interactions between KAI1/CD82 and tetraspanins CD9 and CD151, which also regulate cell movement, but not for the association between KAI1/CD82 and alpha3beta1 integrin. However, KAI1/CD82 still efficiently inhibits cell migration when either CD9 or CD151 is absent. Hence, KAI1/CD82 interacts with tetraspanin and integrin by different mechanisms and is unlikely to inhibit cell migration through its associated proteins. Moreover, without significantly affecting the glycosylation, homodimerization, and global folding of KAI1/CD82, the TM interactions maintain the conformational stability of KAI1/CD82, evidenced by the facts that the mutant is more sensitive to denaturation and less associable with tetraspanins and supported by the modeling analysis. Thus, the TM interactions mediated by these polar residues determine a conformation either in or near the tightly packed TM region and this conformation and/or its change are needed for the intrinsic activity of KAI1/CD82. In contrast to immense efforts to block the signaling of cancer progression, the perturbation of TM interactions may open a new avenue to prevent cancer invasion and metastasis.
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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.