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S100A4 released from highly bone-metastatic breast cancer cells plays a critical role in osteolysis

Bone Research 2019年第4期7卷 424-436页

作者： haemin kim Bongjun kim Sang Il kim Hyung Joon kim Brian YRyu Junho Chung Zang Hee Lee Hong-Hee kim Department of Cell and Developmental Biology BK21 Program and DRISeoul National UniversitySeoulKorea Department of Biochemistry and Molecular Biology Seoul National University College of MedicineSeoulKorea Cancer Research Institute Seoul National University College of MedicineSeoulKorea Department of Cancer Biology Seoul National University College of MedicineSeoulKorea Department of Oral Physiology BK21 PLUS Projectand Dental and Life Science InstituteSchool of DentistryPusan National UniversityYangsanKorea Interdisciplinary Program in Bioinformatics Seoul National University College of Natural SciencesSeoulKorea Department of Biomedical Sciences Seoul National University Graduate SchoolSeoulKorea

Bone destruction induced by breast cancer metastasis causes severe complications,including death,in breast cancer *** between cancer cells and skeletal cells in metastatic bone microenvironments is a principal element that drives tumor progression and ***-derived factors play fundamental roles in this form of *** identify soluble factors released from cancer cells in bone metastasis,we established a highly bone-metastatic subline of MDA-MB-231 breast cancer *** subline(mtMDA)showed a markedly elevated ability to secrete S100A4 protein,which directly stimulated osteoclast formation via surface receptor *** S100A4 stimulated osteoclastogenesis in vitro and bone loss in *** medium from mtMDA cells in which S100A4 was knocked down had a reduced ability to stimulate ***,the S100A4 knockdown cells elicited less bone destruction in mice than the control knockdown *** addition,administration of an anti-S100A4 monoclonal antibody(mAb)that we developed attenuated the stimulation of osteoclastogenesis and bone loss by mtMDA in *** together,our results suggest that S100A4 released from breast cancer cells is an important player in the osteolysis caused by breast cancer bone metastasis.

关键词： S100A4 breast metastatic

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SREBP2 restricts osteoclast differentiation and activity by regulating IRF7 and limits inflammatory bone erosion

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Bone Research 2024年第3期12卷 689-703页

作者： haemin kim In Ah Choi Akio Umemoto Seyeon Bae Kaichi Kaneko Masataka Mizuno Eugenia Giannopoulou Tania Pannellini Liang Deng Kyung-Hyun Park-Min Arthritis and Tissue Degeneration Program David Z.Rosensweig Genomics Research CenterHospital for Special SurgeryNew YorkNY 11366USA Department of Medicine Weill Cornell Medical CollegeNew YorkNY 10021USA CHA Biomedical Research Institute CHA Bundang Medical CenterCHA University School of MedicineSeongnam 13496Republic of Korea Department of Internal Medicine College of MedicineChungbuk National UniversityCheongjuChungbuk 28644Republic of Korea Biological Sciences Department New York City College of TechnologyCity University of New YorkBrooklynNY 11201USA Dermatology Service Department of MedicineMemorial Sloan Kettering Cancer CenterNew YorkNY 10065USA Department of Dermatology Weill Cornell Medical CollegeNew YorkNY 10021USA BCMB Allied Program Weill Cornell Graduate School of Medical SciencesNew YorkNY 10065USA

Osteoclasts are multinucleated bone-resorbing cells,and their formation is tightly regulated to prevent excessive bone ***,the mechanisms by which osteoclast formation is restricted remain incompletely ***,we found that sterol regulatory element binding protein 2(SREBP2)functions as a negative regulator of osteoclast formation and inflammatory bone *** and SREBP2,a key transcription factor for cholesterol biosynthesis,increased in the late phase of osteoclastogenesis.

关键词： SREBP2 incomplete restrict

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Augmenting MNK1/2 activation by c-FMS proteolysis promotes osteoclastogenesis and arthritic bone erosion

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Bone Research 2021年第4期9卷 571-581页

作者： Se Hwan Mun Seyeon Bae Steven Zeng Brian Oh Carmen Chai Matthew Jundong kim haemin kim George Kalliolias Chitra Lekha Dahia Younseo Oh Tae-Hwan kim Jong Dae Ji Kyung-Hyun Park-Min Arthritis and Tissue Degeneration Program David Z.Rosensweig Genomics Research CenterNew YorkNYUSA Tissue Engineering Regeneration and RepairHospital for Special SurgeryNew YorkNYUSA Department of Cell and Developmental Biology Weill Cornell Medical CollegeNew YorkNYUSA BCMB allied program Weill Cornell Graduate School of Medical SciencesNew YorkNYUSA Hanyang University Institute for Rheumatology Research SeoulKorea Department of Rheumatology Hanyang University Hospital for Rheumatic DiseasesSeoulKorea Rheumatology College of MedicineKorea UniversitySeoulKorea Department of Medicine Weill Cornell Medical CollegeNew YorkNYUSA

Osteoclasts are bone-resorbing cells that play an essential role in homeostatic bone remodeling and pathological bone *** colony stimulating factor(M-CSF)is abundant in rheumatoid arthritis(RA).However,the role of M-CSF in arthritic bone erosion is not completely ***,we show that M-CSF can promote osteoclastogenesis by triggering the proteolysis of c-FMS,a receptor for M-CSF,leading to the generation of FMS intracellular domain(FICD)*** levels of FICD fragments positively regulated osteoclastogenesis but had no effect on inflammatory ***,myeloid cell-specific FICD expression in mice resulted in significantly increased osteoclast-mediated bone resorption in an inflammatory arthritis *** FICD formed a complex with DAP5,and the FICD/DAP5 axis promoted osteoclast differentiation by activating the MNK1/2/EIF4E pathway and enhancing NFATcl protein ***,targeting the MNK1/2 pathway diminished arthritic bone *** results identified a novel role of c-FMS proteolysis in osteoclastogenesis and the pathogenesis of arthritic bone erosion.

关键词： osteoclast stimulating 1/2

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RANKL-responsive epigenetic mechanism reprograms macrophages into bone-resorbing osteoclasts

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Cellular & Molecular Immunology 2023年第1期20卷 94-109页

作者： Seyeon Bae Kibyeong kim Keunsoo Kang haemin kim Minjoon Lee Brian Oh Kaichi Kaneko Sungkook Ma Jae Hoon Choi Hojoong Kwak Eun Young Lee Sung Ho Park Kyung-Hyun Park-Min Arthritis and Tissue Degeneration Program David Z.Rosensweig Genomics Research CenterHospital for Special SurgeryNew YorkNY10021USA Department of Medicine Weill Cornell Medical CollegeNew YorkNY10065USA Department of Biological Science Ulsan National Institute of Science&Technology(UNIST)Ulsan44919Republic of Korea Department of Life Science College of Natural SciencesResearch Institute for Natural SciencesHanyang UniversitySeoulKorea Department of Microbiology Dankook UniversityCheonan3116Republic of Korea Department of Molecular Biology and Genetics Cornell UniversityIthacaUSA Division of Rheumatology Department of Internal MedicineSeoul National University College of MedicineSeoulKorea BCMB Allied Program Weill Cornell Graduate School of Medical SciencesNew YorkNY10021USA

Monocyte/macrophage lineage cells are highly plastic and can differentiate into various cells under different environmental stimuli. Bone-resorbing osteoclasts are derived from the monocyte/macrophage lineage in response to receptor activator of NF-κB ligand (RANKL). However, the epigenetic signature contributing to the fate commitment of monocyte/macrophage lineage differentiation into human osteoclasts is largely unknown. In this study, we identified RANKL-responsive human osteoclast-specific superenhancers (SEs) and SE-associated enhancer RNAs (SE-eRNAs) by integrating data obtained from ChIP-seq, ATAC-seq, nuclear RNA-seq and PRO-seq analyses. RANKL induced the formation of 200 SEs, which are large clusters of enhancers, while suppressing 148 SEs in macrophages. RANKL-responsive SEs were strongly correlated with genes in the osteoclastogenic program and were selectively increased in human osteoclasts but marginally presented in osteoblasts, CD4+ T cells, and CD34+ cells. In addition to the major transcription factors identified in osteoclasts, we found that BATF binding motifs were highly enriched in RANKL-responsive SEs. The depletion of BATF1/3 inhibited RANKL-induced osteoclast differentiation. Furthermore, we found increased chromatin accessibility in SE regions, where RNA polymerase II was significantly recruited to induce the extragenic transcription of SE-eRNAs, in human osteoclasts. Knocking down SE-eRNAs in the vicinity of the NFATc1 gene diminished the expression of NFATc1, a major regulator of osteoclasts, and osteoclast differentiation. Inhibiting BET proteins suppressed the formation of some RANKL-responsive SEs and NFATc1-associated SEs, and the expression of SE-eRNA:NFATc1. Moreover, SE-eRNA:NFATc1 was highly expressed in the synovial macrophages of rheumatoid arthritis patients exhibiting high-osteoclastogenic potential. Our genome-wide analysis revealed RANKL-inducible SEs and SE-eRNAs as osteoclast-specific signatures, which may contribute to t

关键词： Osteoclasts super-enhancers enhancer RNAs Rheumatoid arthritis

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