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GDF15 promotes prostate cancer bone metastasis and colonization through osteoblastic CCL2 and RANKL activation 被引量:4
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作者 Jawed Akhtar Siddiqui Parthasarathy Seshacharyulu +10 位作者 Sakthivel Muniyan Ramesh Pothuraju parvez khan Raghupathy Vengoji Sanjib Chaudhary Shailendra Kumar Maurya Subodh Mukund Lele Maneesh Jain Kaustubh Datta Mohd Wasim Nasser Surinder Kumar Batra 《Bone Research》 SCIE CAS CSCD 2022年第1期150-164,共15页
Bone metastases occur in patients with advanced-stage prostate cancer(PCa). The cell-cell interaction between PCa and the bone microenvironment forms a vicious cycle that modulates the bone microenvironment, increases... Bone metastases occur in patients with advanced-stage prostate cancer(PCa). The cell-cell interaction between PCa and the bone microenvironment forms a vicious cycle that modulates the bone microenvironment, increases bone deformities, and drives tumor growth in the bone. However, the molecular mechanisms of PCa-mediated modulation of the bone microenvironment are complex and remain poorly defined. Here, we evaluated growth differentiation factor-15(GDF15) function using in vivo preclinical PCa-bone metastasis mouse models and an in vitro bone cell coculture system. Our results suggest that PCa-secreted GDF15 promotes bone metastases and induces bone microarchitectural alterations in a preclinical xenograft model. Mechanistic studies revealed that GDF15 increases osteoblast function and facilitates the growth of PCa in bone by activating osteoclastogenesis through osteoblastic production of CCL2 and RANKL and recruitment of osteomacs. Altogether, our findings demonstrate the critical role of GDF15 in the modulation of the bone microenvironment and subsequent development of PCa bone metastasis. 展开更多
关键词 GDF15 METASTASIS RANKL
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