KDM4C Promotes Proliferation and Migration of Multiple Myeloma Cells by Up-Regulating JAG1 Gene Expression

IF 0.3 4区 医学 Q4 ENGINEERING, BIOMEDICAL Journal of Hard Tissue Biology Pub Date : 2021-01-01 DOI:10.2485/jhtb.30.257
Dan Yu, Min Hu, Qiang Tian
{"title":"KDM4C Promotes Proliferation and Migration of Multiple Myeloma Cells by Up-Regulating JAG1 Gene Expression","authors":"Dan Yu, Min Hu, Qiang Tian","doi":"10.2485/jhtb.30.257","DOIUrl":null,"url":null,"abstract":": Multiple myeloma is a frequent hematological malignancy. Although progress has been made in therapeutic strat-egies, the prognosis of multiple myeloma is far from satisfactory. Therefore, it is imperative to investigate the precise mechanism of multiple myeloma progression. Lysine Demethylase 4C (KDM4C) was demonstrated to be a vital regulator in cancers, while its action on multiple myeloma remains elusive. Thus, we aimed to investigate the effect of KDM4C on multiple myeloma progression and explored the precise mechanism of action. In this study, 70 multiple myeloma patients and 45 normal donors (volunteers) were enrolled. Results showed that KDM4C was highly expressed in plasma of 70 multiple myeloma patients and multiple myeloma cells. Knockdown of KDM4C suppressed proliferation and migration of multiple myeloma cells. Besides, JAG1 expression was enhanced in plasma of 70 myeloma patients and multiple myeloma cells. JAG1 expression was positively correlated with KDM4C expression. Furthermore, KDM4C knockdown suppressed Notch signaling proteins Notch-1, NICD-1, and Hes-1 in multiple myeloma. Moreover, KDM4C knockdown suppressed the proliferation and migration of multiple myeloma cells through down-regulating JAG1 expression. Collectively, KDM4C promotes the proliferation and migration of multiple myeloma cells by up-regulating JAG1 gene expression. KDM4C may be a promising target for multiple myeloma therapy. regulation aggressive behav iors studied and siRNA against co-transfected into multiple myeloma cells. revealed knockdown of ability but abrogated The effect of JAG1 on multiple myeloma cell prolifera and","PeriodicalId":16040,"journal":{"name":"Journal of Hard Tissue Biology","volume":"1 1","pages":""},"PeriodicalIF":0.3000,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Hard Tissue Biology","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.2485/jhtb.30.257","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"ENGINEERING, BIOMEDICAL","Score":null,"Total":0}
引用次数: 0

Abstract

: Multiple myeloma is a frequent hematological malignancy. Although progress has been made in therapeutic strat-egies, the prognosis of multiple myeloma is far from satisfactory. Therefore, it is imperative to investigate the precise mechanism of multiple myeloma progression. Lysine Demethylase 4C (KDM4C) was demonstrated to be a vital regulator in cancers, while its action on multiple myeloma remains elusive. Thus, we aimed to investigate the effect of KDM4C on multiple myeloma progression and explored the precise mechanism of action. In this study, 70 multiple myeloma patients and 45 normal donors (volunteers) were enrolled. Results showed that KDM4C was highly expressed in plasma of 70 multiple myeloma patients and multiple myeloma cells. Knockdown of KDM4C suppressed proliferation and migration of multiple myeloma cells. Besides, JAG1 expression was enhanced in plasma of 70 myeloma patients and multiple myeloma cells. JAG1 expression was positively correlated with KDM4C expression. Furthermore, KDM4C knockdown suppressed Notch signaling proteins Notch-1, NICD-1, and Hes-1 in multiple myeloma. Moreover, KDM4C knockdown suppressed the proliferation and migration of multiple myeloma cells through down-regulating JAG1 expression. Collectively, KDM4C promotes the proliferation and migration of multiple myeloma cells by up-regulating JAG1 gene expression. KDM4C may be a promising target for multiple myeloma therapy. regulation aggressive behav iors studied and siRNA against co-transfected into multiple myeloma cells. revealed knockdown of ability but abrogated The effect of JAG1 on multiple myeloma cell prolifera and
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
KDM4C通过上调JAG1基因表达促进多发性骨髓瘤细胞增殖和迁移
多发性骨髓瘤是一种常见的血液系统恶性肿瘤。尽管在治疗策略方面取得了进展,但多发性骨髓瘤的预后远不能令人满意。因此,研究多发性骨髓瘤进展的确切机制势在必行。赖氨酸去甲基化酶4C (KDM4C)被证明是癌症的重要调节因子,但其对多发性骨髓瘤的作用尚不清楚。因此,我们旨在研究KDM4C对多发性骨髓瘤进展的影响,并探讨其确切的作用机制。本研究纳入70例多发性骨髓瘤患者和45例正常供体(志愿者)。结果显示,70例多发性骨髓瘤患者血浆及多发性骨髓瘤细胞中高表达KDM4C。敲低KDM4C可抑制多发性骨髓瘤细胞的增殖和迁移。此外,JAG1在70例骨髓瘤患者及多发性骨髓瘤细胞的血浆中表达增强。JAG1表达与KDM4C表达呈正相关。此外,KDM4C敲低可抑制多发性骨髓瘤中Notch信号蛋白Notch-1、NICD-1和Hes-1。KDM4C敲低通过下调JAG1的表达抑制多发性骨髓瘤细胞的增殖和迁移。总的来说,KDM4C通过上调JAG1基因表达促进多发性骨髓瘤细胞的增殖和迁移。KDM4C可能是多发性骨髓瘤治疗的一个有希望的靶点。并将siRNA共转染到多发性骨髓瘤细胞中。结果表明,JAG1对多发性骨髓瘤细胞增殖的抑制作用明显减弱,但对骨髓瘤细胞增殖的抑制作用明显减弱
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Journal of Hard Tissue Biology
Journal of Hard Tissue Biology ENGINEERING, BIOMEDICAL-
CiteScore
0.90
自引率
0.00%
发文量
28
审稿时长
6-12 weeks
期刊介绍: Information not localized
期刊最新文献
Evaluation of Maxillary First Molar Intrusion Mechanics with Mini-Implant Anchorages Using the Finite Element Method Study on the Effect of Soft-Start Light on Microleakage in Pit and Fissure Closure Upregulation of miR-101-3p Overcomes Ibrutinib Resistance by Targeting ABCC5 in Diffuse Large B-Cell Lymphoma (DLBCL) miR-141 Improve Osteoporosis by Promoting Osteoblast Differentiation through Targeting RICTOR A Study of Submandibular Gland Changes in Mice of a Murine Model of Sjögren’s Syndrome Administered Dental Pulp Stem Cell-Conditioned Medium
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1