{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T03:18:57Z","timestamp":1779160737296,"version":"3.51.4"},"reference-count":39,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2015,2,25]],"date-time":"2015-02-25T00:00:00Z","timestamp":1424822400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2015,6]]},"abstract":"<jats:sec><jats:label\/><jats:p>Osteolytic bone diseases are characterized by excessive osteoclast formation and activation. Protein kinase C (PKC)\u2010dependent pathways regulate cell growth, differentiation and apoptosis in many cellular systems, and have been implicated in cancer development and osteoclast formation. A number of PKC inhibitors with anti\u2010cancer properties have been developed, but whether they might also influence osteolysis (a common complication of bone invading cancers) is unclear. We studied the effects of the PKC inhibitor compound, GF109203X on osteoclast formation and activity, processes driven by receptor activator of NF\u03baB ligand (RANKL). We found that GF109203X strongly and dose dependently suppresses osteoclastogenesis and osteoclast activity in RANKL\u2010treated primary mouse bone marrow cells. Consistent with this GF109203X reduced expression of key osteoclastic genes, including cathepsin K, calcitonin receptor, tartrate resistant acid phosphatase (TRAP) and the proton pump subunit V\u2010ATPase\u2010d2 in RANKL\u2010treated primary mouse bone marrow cells. Expression of these proteins is dependent upon RANKL\u2010induced NF\u2010\u03baB and NFAT transcription factor actions; both were reduced in osteoclast progenitor populations by GF109203X treatment, notably NFATc1 levels. Furthermore, we showed that GF109203X inhibits RANKL\u2010induced calcium oscillation. Together, this study shows GF109203X may block osteoclast functions, suggesting that pharmacological blockade of PKC\u2010dependent pathways has therapeutic potential in osteolytic diseases. J. Cell. Physiol. 230: 1235\u20131242, 2015. \u00a9 2014 Wiley Periodicals, Inc., A Wiley Company<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcp.24858","type":"journal-article","created":{"date-parts":[[2014,11,3]],"date-time":"2014-11-03T05:59:15Z","timestamp":1414994355000},"page":"1235-1242","source":"Crossref","is-referenced-by-count":21,"title":["Protein Kinase C Inhibitor, GF109203X Attenuates Osteoclastogenesis, Bone Resorption and RANKL\u2010Induced NF\u2010\u03baB and NFAT Activity"],"prefix":"10.1002","volume":"230","author":[{"given":"Jun","family":"Yao","sequence":"first","affiliation":[{"name":"Department of Orthopaedic Surgery Research Centre for Regenerative Medicine The First Affiliated Hospital of Guangxi Medical University Guangxi China"},{"name":"School of Pathology and Laboratory Medicine The University of Western Australia Perth Western Australia 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