维普中文期刊产品整合服务
共被期刊论文引用了5次 您的检索式:您选中1篇文献正在查看引证文献汇总
    题名 作者 年代 出处 被引量
1DCZ0801,a novel compound,induces cell apoptosis and cell cycle arrest via MAPK pathway in multiple myeloma显示文摘Multiple myeloma(MM)is a refractory malignant hematological malignancy,and many therapeutic strategies have been developed to cure patients with MM.DCZ0801 is a compound that consists of oxophenamide and pterostilbene.The role of these compounds in hematological cancers such as MM has yet to be studied.In this study,we explored the potential mechanism of DCZ0801 action,its anti-tumor activity both in vitro and in vivo on MM.This study was carried out via cell cycle proliferation assay,apoptotic analysis,western blot analysis,and examination of xenotransplantation model of tumors.The in vitro studies revealed that DCZ0801 could inhibit cell proliferation and induce apoptosis by regulating both caspase-dependent and mitogen-activated protein kinase signaling pathways,inducing S-phase arrest of the cell cycle related to downregulation of CDK2,cyclin-A2,and CDC25A protein expression.The in vivo studies showed that DCZ0801 could significantly reduce the size of the tumors in nude mice.Our results demonstrated that DCZ0801 may emerge as the new therapeutic option for the patient with MM.Ting Zhang Bo Li Qilin Feng Zhijian Xu Cheng Huang Huiqun Wu Zhangbo Chen Liangning Hu Lu Gao Peng Liu Guang Yang Hui Zhang Kang Lu Tingye Li Yi Tao Xiaosong Wu Jumei Shi Weiliang Zhu 2019Acta Biochimica et Biophysica Sinica2019,51,5:3
2炎症小体在恶性血液病发病中的作用显示文摘炎症小体是一类胞质内多蛋白复合体,组装后活化半胱氨酸天氰冬氨酸蛋白酶(caspase)-1,进而介导白细胞介素(IL)-1β、IL-18等细胞因子的成熟和释放。随着对炎症小体的深入研究,炎症小体除启动炎症反应外,也参与恶性肿瘤的发生、发展、转移及预后。炎症小体组分及其诱导产生细胞因子IL-1β、IL-18在不同恶性血液病中表达、作用及机制各异。王金霞 刘爱飞 李方林 陈懿建 2017中国老年学杂志2017,37,16:2
3雷公藤抗多发性骨髓瘤研究进展显示文摘雷公藤具有广泛的抗炎、免疫抑制及抗肿瘤等作用。近年在抗多发性骨髓瘤(MM)的研究中发现,其主要药效成分为雷公藤甲素(TPL)及雷公藤红素(Celastrol)。通过综述TPL及Celastrol的抗MM作用机制,发现二者均有良好的抑制MM细胞增殖、诱导凋亡的作用,但也存在不同点。二者作为同一中药的不同组分,如何在MM治疗中协同发挥作用、会不会产生竞争性抑制,目前尚不甚清楚,二者的毒副作用控制方面还需进一步研究。顾恪波 何立丽 张丽娜 吴洁 张晨 孙岸弢 张明辉 2019河北中医2019,41,5:2
4炎性复合体在恶性血液病中的作用及研究进展显示文摘炎性复合体是细胞内多种蛋白质组成的蛋白复合体,主要存在于单核细胞、巨噬细胞等髓系细胞胞质中。其概念首先由Martinon等^[1]于2002年提出。炎性复合体是固有免疫系统结构和功能的基本单元之一,可以识别或感知病原体/损伤相关分子模式、激活白细胞介素(IL)1β和IL-1β、介导一系列免疫应答^[2]。多种肿瘤的生物学行为与活化的炎症复合体相关。王嘉 赵明峰 2018中华医学杂志2018,98,40:0
5Dihydrocelastrol induces antitumor activity and enhances the sensitivity of bortezomib in resistant multiple myeloma by inhibiting STAT3-dependent PSMB5 regulation显示文摘Multiple myeloma(MM)is characterized by excessive aggregation of B-cell-derived malignant plasma cells in the hematopoietic system of bone marrow.Previously,we synthesized an innovative molecule named dihydrocelastrol(DHCE)from celastrol,a triterpene purified from medicinal plant Tripterygium wilfordii.Herein,we explore the therapeutic properties and latent signal transduction mechanism of DHCE action in bortezomib(BTZ)-resistant(BTZ-R)MM cells.In this study,we first report that DHCE shows antitumor activities in vitro and in vivo and exerts stronger inhibitory effects than celastrol on BTZ-R cells.We find that DHCE inhibits BTZ-R cell viability by promoting apoptosis via extrinsic and intrinsic pathways and suppresses BTZ-R MM cell proliferation by inducing G0/G1 phase cell cycle arrest.In addition,inactivation of JAK2/STAT3 and PI3K/Akt pathways are involved in the DHCE-mediated antitumor effect.Simultaneously,DHCE acts synergistically with BTZ on BTZ-R cells.PSMB5,a molecular target of BTZ,is overexpressed in BTZ-R MM cells compared with BTZ-S MM cells and is demonstrated to be a target of STAT3.Moreover,DHCE downregulates PSMB5 overexpression in BTZ-R MM cells,which illustrates that DHCE overcomes BTZ resistance through increasing the sensitivity of BTZ in resistant MM via inhibiting STAT3-dependent PSMB5 regulation.Overall,our findings imply that DHCE may become a potential therapeutic option that warrants clinical evaluation for BTZ-R MM.Shuhan Jin Bo Li Bibo Zhang Xuejie Gao Xinyan Jia Li Xu Shuaikang Chang Ke Hu Guanli Wang Zhijian Xu Ting Zhang Dongliang Song Guang Yang Xiaosong Wu Huabin Zhu Cheng Huang Yumeng Lu Jumei Shi Weiliang Zhu Gege Chen 2023Acta Biochimica et Biophysica Sinica2023,55,12:0
返回顶部 每页显示:
共1页 首页 上一页 第1页 下一页 末页 /1 跳转

网站首页 | 关于我们 | 联系我们 | 产品服务 | 客服中心 | 广告服务 | 版权声明 | 网站联盟 | 友情链接 | 售卡网点

版权所有© 渝B2-20050021-1 渝公网安备 50019002500403号 违法和不良信息举报中心

互联网出版许可证 新出网证(渝)字10号 全国400电话 - 免长途话费