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Artemisinin-Daumone Hybrid Inhibits Cancer Cell-Mediated Osteolysis by Targeting Cancer Cells and Osteoclasts

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dc.contributor.author박광균-
dc.contributor.author박준희-
dc.contributor.author이선경-
dc.contributor.author정원윤-
dc.date.accessioned2018-10-11T08:56:16Z-
dc.date.available2018-10-11T08:56:16Z-
dc.date.issued2018-
dc.identifier.issn1015-8987-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/163482-
dc.description.abstractBACKGROUND/AIMS: Bone metastasis of cancer cells decreases patient survival and quality of life. Hybridization via the covalent coupling of two bioactive natural products is a useful strategy for developing more potent anticancer agents by enhancing their bioavailability and avoiding drug resistance. METHODS: The in vivo activities of artemisinin-daumone hybrid 15 (ARTD) were estimated in cancer cell-inoculated mice and ovariectomized mice. The viability, migration, and invasion of cancer cells were measured via MTT, wound-healing, and transwell invasion assays. ARTD-regulated transcription factors were detected with an RT2 profiler PCR array kit and Western blotting. Osteoclastogenesis and osteoclast activity were detected with tartrate-resistant acid phosphatase staining, a pit formation assay, gelatin zymography, and a cathepsin K ELISA assay. RESULTS: ARTD blocked cancer-associated osteolysis more potently than artemisinin in mice with intratibially inoculated breast cancer or lung cancer cells. ARTD inhibited the viability, migration, and invasion of breast and lung cancer cells in the absence or presence of transforming growth factor-β1. ARTD treatment induced the expression of tumor suppressive activating transcription factor 3 and inhibited oncogenic E2F transcription factor 1 expression at the mRNA and protein levels. ARTD inhibited receptor activator of nuclear factor kappa-B ligand-induced osteoclast formation and bone resorbing activity by reducing the secreted levels of matrix metalloproteinase-9 and cathepsin K. Furthermore, ARTD prevented estrogen deficiency-induced bone loss in ovariectomized mice. CONCLUSION: ARTD may be a promising candidate for inhibiting cancer-induced bone destruction. The application of ARTD may be extended to patients with chemotherapy-induced ovarian failure or postmenopausal osteoporosis.-
dc.description.statementOfResponsibilityopen-
dc.formatapplication/pdf-
dc.languageEnglish-
dc.publisherS. Karger-
dc.relation.isPartOfCELLULAR PHYSIOLOGY AND BIOCHEMISTRY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleArtemisinin-Daumone Hybrid Inhibits Cancer Cell-Mediated Osteolysis by Targeting Cancer Cells and Osteoclasts-
dc.typeArticle-
dc.contributor.collegeCollege of Dentistry-
dc.contributor.departmentDept. of Oral Biology-
dc.contributor.googleauthorGwang Taek Ma-
dc.contributor.googleauthorSun Kyoung Lee-
dc.contributor.googleauthorKwang-Kyun Park-
dc.contributor.googleauthorJunhee Park-
dc.contributor.googleauthorSeung Hwa Son-
dc.contributor.googleauthorMankil Jung-
dc.contributor.googleauthorWon-Yoon Chung-
dc.identifier.doi10.1159/000493449-
dc.contributor.localIdA01429-
dc.contributor.localIdA01677-
dc.contributor.localIdA02854-
dc.contributor.localIdA03676-
dc.relation.journalcodeJ00501-
dc.identifier.eissn1421-9778-
dc.identifier.pmid30205376-
dc.subject.keywordArtemisinin-
dc.subject.keywordBone metastasis-
dc.subject.keywordCancer-associated osteolysis-
dc.subject.keywordDaumone-
dc.subject.keywordHybrid molecules-
dc.contributor.alternativeNamePark, Kwang Kyun-
dc.contributor.alternativeNamePark, Jun Hee-
dc.contributor.alternativeNameLee, Seon Kyung-
dc.contributor.alternativeNameChung, Won Yoon-
dc.contributor.affiliatedAuthorPark, Kwang Kyun-
dc.contributor.affiliatedAuthorPark, Jun Hee-
dc.contributor.affiliatedAuthorLee, Seon Kyung-
dc.contributor.affiliatedAuthorChung, Won Yoon-
dc.citation.volume49-
dc.citation.number4-
dc.citation.startPage1460-
dc.citation.endPage1475-
dc.identifier.bibliographicCitationCELLULAR PHYSIOLOGY AND BIOCHEMISTRY, Vol.49(4) : 1460-1475, 2018-
Appears in Collections:
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers
5. Research Institutes (연구소) > Oral Cancer Research Institute (구강종양연구소) > 1. Journal Papers

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