• Find People
  • Campus Map
  • PiratePort
  • A-Z
    • About
    • Submit
    • Browse
    • Login
    View Item 
    •   ScholarShip Home
    • Other Campus Research
    • Open Access
    • View Item
    •   ScholarShip Home
    • Other Campus Research
    • Open Access
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Browse

    All of The ScholarShipCommunities & CollectionsDateAuthorsTitlesSubjectsTypeDate SubmittedThis CollectionDateAuthorsTitlesSubjectsTypeDate Submitted

    My Account

    Login

    Statistics

    View Google Analytics Statistics

    The claudin family of proteins in human malignancy: A clinical perspective

    Thumbnail
    View/ Open
    cmar-5-367.pdf (389.2Kb)

    Show full item record
    Author
    Ding, Lei; Lu, Zhe; Lu, Qun; Chen, Yan-Hua
    Abstract
    Tight junctions, or zonula occludens, are the most apical component of the junctional complex and provide one form of cell–cell adhesion in epithelial and endothelial cells. Nearly 90% of malignant tumors are derived from the epithelium. Loss of cell–cell adhesion is one of the steps in the progression of cancer to metastasis. At least three main tight junction family proteins have been discovered: occludin, claudin, and junctional adhesion molecule (JAM). Claudins are the most important structural and functional components of tight junction integral membrane proteins, with at least 24 members in mammals. They are crucial for the paracellular flux of ions and small molecules. Overexpression or downregulation of claudins is frequently observed in epithelial-derived cancers. However, molecular mechanisms by which claudins affect tumorigenesis remain largely unknown. As the pivotal proteins in epithelial cells, altered expression and distribution of different claudins have been reported in a wide variety of human malignancies, including pancreatic, colonic, lung, ovarian, thyroid, prostate, esophageal, and breast cancers. In this review, we will give the readers an overall picture of the changes in claudin expression observed in various cancers and their mechanisms of regulation. Downregulation of claudins contributes to epithelial transformation by increasing the paracellular permeability of nutrients and growth factors to cancerous cells. In the cases of upregulation of claudin expression, the barrier function of the cancerous epithelia changes, as they often display a disorganized arrangement of tight junction strands with increased permeability to paracellular markers. Finally, we will summarize the literature suggesting that claudins may become useful biomarkers for cancer detection and diagnosis as well as possible therapeutic targets for cancer treatment.
    URI
    http://hdl.handle.net/10342/7800
    Subject
    tight junctions, claudins, human cancers
    Date
    2013-10-07
    Citation:
    APA:
    Ding, Lei, & Lu, Zhe, & Lu, Qun, & Chen, Yan-Hua. (October 2013). The claudin family of proteins in human malignancy: A clinical perspective. , (), - . Retrieved from http://hdl.handle.net/10342/7800

    Display/Hide MLA, Chicago and APA citation formats.

    MLA:
    Ding, Lei, and Lu, Zhe, and Lu, Qun, and Chen, Yan-Hua. "The claudin family of proteins in human malignancy: A clinical perspective". . . (), October 2013. September 27, 2023. http://hdl.handle.net/10342/7800.
    Chicago:
    Ding, Lei and Lu, Zhe and Lu, Qun and Chen, Yan-Hua, "The claudin family of proteins in human malignancy: A clinical perspective," , no. (October 2013), http://hdl.handle.net/10342/7800 (accessed September 27, 2023).
    AMA:
    Ding, Lei, Lu, Zhe, Lu, Qun, Chen, Yan-Hua. The claudin family of proteins in human malignancy: A clinical perspective. . October 2013; (): . http://hdl.handle.net/10342/7800. Accessed September 27, 2023.
    Collections
    • Open Access

    xmlui.ArtifactBrowser.ItemViewer.elsevier_entitlement

    East Carolina University has created ScholarShip, a digital archive for the scholarly output of the ECU community.

    • About
    • Contact Us
    • Send Feedback