Therapeutic effects of thalidomide in myeloma are associated with the expression of fibroblast growth factor receptor 3.

成纤维细胞生长因子受体3 转染 癌症研究 细胞生长 成纤维细胞生长因子 克隆(Java方法) MAPK/ERK通路 成纤维细胞生长因子受体2 分子生物学 生长因子 血管内皮生长因子 成纤维细胞生长因子受体 成纤维细胞生长因子受体4 信号转导 生物 受体 医学 细胞培养 内科学 细胞生物学 DNA 生物化学 遗传学 血管内皮生长因子受体
作者
Shenxian Qian,George Somlo,Bingsen Zhou,Yun Yen
出处
期刊:PubMed 被引量:6
链接
标识
摘要

Thalidomide (Thal), a novel agent in the treatment of multiple myeloma, is presumed to act through a variety of mechanisms. In the present study, we examined the relationship between fibroblast growth factor receptor 3 (FGFR3) expression and the therapeutic effect of Thal. The DNA synthesis of KMS-11 clone, which overexpresses FGFR3, was inhibited by Thal in a dose-dependent manner; whereas U266 cells, which lack FGFR3 expression, failed to respond to Thal inhibition. To further examine the intertwining of Thal's therapeutic effects, wild-type human full-length FGFR3 cDNA was transfected into U266 cells. FGFR3 transfected U266 clones revealed increased FGFR3 expression, but resulted in decreased DNA synthesis and increased apoptosis under Thal treatment. Under Thal treatment, the myeloma proliferation-related protein, vascular endothelial growth factor (VEGF), and interleukin-6 (IL-6) were decreased in U266 FGFR3 transfectant as well. These results suggest that Thal inhibits myeloma cell proliferation and may depend on FGFR3 expression status. To further confirm this observation, we transfected a plasmid constructed anti-FGFR3 ribozyme (Rz52) into KMS-11 cells. In the ribozyme transfectant KMS-11 clone, FGFR3 expression was decreased; whereas the effects of Thal in cell growth inhibition were abrogated in KMS-11 Rz52 clone. Further results suggested that Thal inhibition of DNA synthesis, induction of apoptosis, and down-regulation of VEGF and IL-6 might be dependent on FGFR3-associated signal transduction of the ERK and STAT3 phosphorylation pathway. Thus, FGFR3 may be a predictive/surrogate marker for selection of Thal treatment in myeloma.

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
PDF的下载单位、IP信息已删除 (2025-6-4)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
研友_VZG7GZ应助积极灵薇采纳,获得10
刚刚
JamesPei应助无限飞丹采纳,获得10
刚刚
独特乘云发布了新的文献求助10
刚刚
科研通AI2S应助科研通管家采纳,获得10
刚刚
科目三应助科研通管家采纳,获得10
刚刚
酷波er应助科研通管家采纳,获得10
刚刚
科研通AI5应助科研通管家采纳,获得10
刚刚
搜集达人应助科研通管家采纳,获得10
刚刚
CAOHOU应助科研通管家采纳,获得10
1秒前
1秒前
CodeCraft应助科研通管家采纳,获得10
1秒前
CodeCraft应助科研通管家采纳,获得10
1秒前
Noyo应助科研通管家采纳,获得10
1秒前
科研通AI2S应助科研通管家采纳,获得10
1秒前
tramp应助科研通管家采纳,获得10
1秒前
英俊的铭应助科研通管家采纳,获得10
1秒前
tramp应助科研通管家采纳,获得10
1秒前
英姑应助科研通管家采纳,获得10
1秒前
1秒前
1秒前
2秒前
领导范儿应助Nozomi采纳,获得10
4秒前
小马甲应助YJ888采纳,获得10
4秒前
香蕉觅云应助jialiu采纳,获得10
4秒前
cosmos完成签到,获得积分10
5秒前
大个应助独特乘云采纳,获得10
6秒前
6秒前
小晓发布了新的文献求助10
6秒前
wonder123发布了新的文献求助10
8秒前
老实起哞完成签到,获得积分10
8秒前
10秒前
11秒前
gsj发布了新的文献求助10
12秒前
13秒前
所所应助wonder123采纳,获得10
13秒前
14秒前
14秒前
14秒前
田様应助忆茶戏采纳,获得10
14秒前
wss完成签到,获得积分10
15秒前
高分求助中
A new approach to the extrapolation of accelerated life test data 1000
ACSM’s Guidelines for Exercise Testing and Prescription, 12th edition 500
‘Unruly’ Children: Historical Fieldnotes and Learning Morality in a Taiwan Village (New Departures in Anthropology) 400
Indomethacinのヒトにおける経皮吸収 400
Phylogenetic study of the order Polydesmida (Myriapoda: Diplopoda) 370
基于可调谐半导体激光吸收光谱技术泄漏气体检测系统的研究 350
Robot-supported joining of reinforcement textiles with one-sided sewing heads 320
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 遗传学 基因 物理化学 催化作用 冶金 细胞生物学 免疫学
热门帖子
关注 科研通微信公众号,转发送积分 3989444
求助须知:如何正确求助?哪些是违规求助? 3531531
关于积分的说明 11254250
捐赠科研通 3270191
什么是DOI,文献DOI怎么找? 1804901
邀请新用户注册赠送积分活动 882105
科研通“疑难数据库(出版商)”最低求助积分说明 809174