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Identification of cancer-derived mediators of bone metastasis and osteolysis may lead to novel therapeutic strategies. In this study, we established highly bone-metastatic PC3 prostate and MDA-MB-231 (MDA) breast cancer cell sublines by in vivo selection in mice. In bone-metastatic cancer cells, the expression and secretion of connective tissue growth factor (CTGF) were highly upregulated. CTGF knockdown in bone-metastatic cells decreased invasion activity and MMP expression. RUNX2 overexpression in the CTGF knockdown cells restored the invasion activity and MMP expression. In addition, CTGF increased RUNX2 protein stability by inducing its acetylation via p300 acetyl transferase. The integrin \u03b1v\u03b23 receptor mediated these effects of CTGF. Furthermore, CTGF promoted RUNX2 recruitment to the RANKL promoter, resulting in increased RANKL production from the tumor cells and subsequent stimulation of osteoclastogenesis from precursor cells. In addition, animal model with injection of CTGF knocked-down prostate cancer cells into 6-week old BALB\/c male mice showed reduced osteolytic lesions. More importantly, the expression levels of CTGF and RANKL showed a strong positive correlation in human primary breast tumor tissues and were higher in bone metastases than in other site metastases. These findings indicate that CTGF plays crucial roles for osteolytic bone metastasis both by enhancing invasiveness of tumor cells and by producing RANKL for osteoclastogenesis. Targeting CTGF may lead to the development of effective preventive and therapeutic strategies for osteolytic metastasis. \u00a9 2019 American Society for Bone and Mineral Research.<\/jats:p>","DOI":"10.1002\/jbmr.3869","type":"journal-article","created":{"date-parts":[[2019,9,10]],"date-time":"2019-09-10T16:13:45Z","timestamp":1568132025000},"page":"155-166","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":70,"title":["A CTGF-RUNX2-RANKL Axis in Breast and Prostate Cancer Cells Promotes Tumor Progression in Bone"],"prefix":"10.1093","volume":"35","author":[{"given":"Bongjun","family":"Kim","sequence":"first","affiliation":[{"name":"Department of Cell and Developmental Biology, BK21 Program and DRI Seoul National University, School of Dentistry Seoul South Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haemin","family":"Kim","sequence":"additional","affiliation":[{"name":"Arthritis and Tissue Degeneration Program, David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery\/Weill Cornell Medicine New York NY USA"},{"name":"Department of Cell and Developmental Biology, BK21 Program and DRI Seoul National University, School of Dentistry Seoul South Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Suhan","family":"Jung","sequence":"additional","affiliation":[{"name":"Department of Cell and Developmental Biology, BK21 Program and DRI Seoul National University, School of Dentistry Seoul South Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aree","family":"Moon","sequence":"additional","affiliation":[{"name":"College of Pharmacy Duksung Women's University Seoul South Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dong-Young","family":"Noh","sequence":"additional","affiliation":[{"name":"Department of Surgery and Cancer Research Institute College of Medicine, Seoul National University Seoul South 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