Details

Autor(en) / Beteiligte

• Tate, Amanda W.
• Lung, Tina
• Radhakrishnan, Anu
• Lim, So Dug
• Lin, Xi
• Edlund, Magnus

Titel

Changes in gap junctional connexin isoforms during prostate cancer progression

Ist Teil von

• The Prostate, 2006-01, Vol.66 (1), p.19-31

Ort / Verlag

Hoboken: Wiley Subscription Services, Inc., A Wiley Company

Erscheinungsjahr

2006

Quelle

Wiley Online Library All Journals

Beschreibungen/Notizen

• BACKGROUND Connexins have their traditional function as part of gap junction (GJ) structures, but have recently been shown to have GJ‐independent roles. Although GJs and their connexin subunits are thought to be down‐regulated in cancer, depending on the connexin examined, many times the expression level is preserved or even increased. This is further apparent by the importance of GJs in “by‐stander effects” of radiation and viral targeting treatments. METHODS We surveyed connexin isoforms in prostate cancer cell lines and tissue with RT‐PCR and immunohistochemistry. Upon modulating GJ function, we observed prostate epithelial cell behaviors. RESULTS Advanced cells within PC‐3 and LNCaP prostate cancer progression models exhibit elevated connexin 26 (Cx26) levels—a trend validated in clinical samples. When GJs were inhibited, adhesion was not affected, but invasion and migration were strikingly decreased. A link between the expression of Cx26 and integrin adhesion‐linked functions are suggested by Cx26's direct interaction with focal adhesion kinase (FAK). CONCLUSIONS These results suggest a novel mechanism for adhesion regulation by a GJ‐independent Cx26 function that correlates with prostate disease progression. The increased Cx26 expression during prostate cancer progression plays a role in adhesion regulation possibly through its interaction with FAK. © 2005 Wiley‐Liss, Inc.