Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8299834 | Biochimica et Biophysica Acta (BBA) - Biomembranes | 2018 | 54 Pages |
Abstract
Over the past 50Â years, increasing experimental evidences have established that connexins (Cxs) and gap junctional intercellular communication (GJIC) ensure an important role in both the onset and development of cancerous processes. In the present review, we focus on the impact of Cxs and GJIC during the development of prostate cancer (PCa), from the primary growth mainly localized in acinar glands and ducts to the distant metastasis mainly concentrated in bone. As observed in several other types of solid tumours, Cxs and especially Cx43 exhibit an ambivalent role with a tumour suppressor effect in the early stages and, conversely, a rather pro-tumoural profile for most of invasion and dissemination steps to secondary sites. We report here the current knowledge on the function of Cxs during PCa cells migration, cytoskeletal dynamics, proteinases activities and the cross talk with the surrounding stromal cells in the microenvironment of the tumour and the bones. In addition, we discuss the role of Cxs in the bone tropism even if the prostate model is rarely used to study the complete sequence of cancer dissemination compared to breast cancer or melanoma. Even if not yet fully understood, these recent findings on Cxs provide new insights into their molecular mechanisms associated with progression and bone targeted behaviour of PCa. This article is part of a Special Issue entitled: Gap Junction Proteins edited by Jean Claude Herve.
Keywords
TSAECMGJICCBXCXCR4BMECHDACAGAFAKRANKLRUNX2CXCL12Connexin43PSAMMPbone marrow endothelial cellsCSCtwist-related protein 1ODDDGJA1DHTHSCmiRNA or miRC-X-C motif chemokine 12uPARuPAprostatic intraepithelial neoplasiaPCAALPAlkaline phosphatasegap junctional intercellular communicationOsteoblastsTrichostatin AInvasionEMTDihydrotestosteroneRankTIMPProstate cancerHematopoietic stem cellCancer stem cellsRunt-related transcription factor 2urokinase plasminogen activatorExtracellular matrixmatrix metalloproteinaseBone metastasisMigrationTissue inhibitor of metalloproteinaseMicroRNAC-X-C chemokine receptor type 4Benign prostatic hyperplasiaBPHprostate-specific antigenPINTwistcarbenoxoloneconnexinfocal adhesion kinaseepithelial-to-mesenchymal transitionuPA receptor
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Authors
Jonathan Boucher, Arnaud Monvoisin, Justine Vix, Marc Mesnil, Dominique Thuringer, Françoise Debiais, Laurent Cronier,