Abstract
Communication among cells via direct cell-cell contact by connexin gap junctions, or between cell and extracellular environment via pannexin channels or connexin hemichannels, is a key factor in cell function and tissue homeostasis. Upon malignant transformation in different cancer types, the dysregulation of these connexin and pannexin channels and their effect in cellular communication, can either enhance or suppress tumorigenesis and metastasis. In this review, we will highlight the latest reports on the role of the well characterized connexin family and its ability to form gap junctions and hemichannels in cancer. We will also introduce the more recently discovered family of pannexin channels and our current knowledge about their involvement in cancer progression.
Highlights
Intercellular communication between cells is realized through gap junction channels formed by connexins (Cx)
We will highlight the latest reports on the role of the well characterized connexin family and its ability to form gap junctions and hemichannels in cancer
We have previously shown that mouse melanocytes have low Panx1 expression while the aggressiveness of isogenic melanoma cell lines [167] (B16-FO, F10 and BL6) is directly correlated to their Panx1 levels, with no detectable Panx2 or Panx3 expression [154]
Summary
Intercellular communication between cells is realized through gap junction channels formed by connexins (Cx). Connexin expression is reported to suppress cancer behavior and this function is independent of their roles in forming gap junction and hemichannels [41]. Reduced expression of connexins and gap junctional communication has been shown in many tumor types. In vivo studies demonstrate the tumor suppressive roles of Cx43 and Cx32, in which mice with decreased expression of Cx43 or Cx32 exhibit increased carcinogeninduced tumor growth in comparison to control wild-type mice, represented by an increase in number and size of tumor nodules in the lung [58, 59]. Inhibition of Cx43 gap junctions accelerates proliferation of four different melanoma cell lines whereas as expected, increased coupling through overexpression of Cx43 reduces cell growth and melanoma tumor growth in vivo [61].
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
