• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

维甲酸可诱导伯基特淋巴瘤细胞中c-fgr原癌基因mRNA水平发生变化。

Retinoic acid induces changes in c-fgr proto-oncogene mRNA levels in Burkitt's lymphoma cells.

作者信息

Faulkner L, Katz D R, Brickell P M

机构信息

Department of Biochemistry and Molecular Biology, Bland Sutton Institute, University College and Middlesex School of Medicine, London, United Kingdom.

出版信息

Immunobiology. 1993 Aug;188(4-5):460-8. doi: 10.1016/S0171-2985(11)80227-5.

DOI:10.1016/S0171-2985(11)80227-5
PMID:8244449
Abstract

The c-fgr proto-oncogene is expressed in Burkitt's lymphoma (BL) cell and cell lines derived from them. When Epstein-Barr virus (EBV)-negative BL cell lines that contain low levels of c-fgr mRNA are infected with EBV, transcription of the c-fgr gene is further induced. In this paper we show that treatment of EBV-negative and EBV-positive BL cell lines with all-trans retinoic acid also stimulates an increase in c-fgr mRNA levels, varying between 2- and 13-fold depending on the cell line. An increase is detectable 12 to 48 h after treatment, depending on the cell line, suggesting that the c-fgr gene is not regulated directly by retinoic acid but responds to other retinoic acid-induced changes in the cell. We also show that treatment of BL cell lines with all-trans retinoic acid either results in a dose-dependent decrease in growth rate, or has no effect on growth, depending on the cell line. It has previously been suggested that the c-fgr gene product might have a role in regulating the growth of BL cells, since treatment of the EBV-positive BL cell line Daudi with alpha-interferon results in a decrease in c-fgr mRNA levels followed by a decrease in growth rate. Our data indicate that there is no general correlation between c-fgr mRNA levels and growth rate in BL cells and so argue against a role for the c-fgr gene product in growth regulation in these cells.

摘要

原癌基因c-fgr在伯基特淋巴瘤(BL)细胞及其衍生的细胞系中表达。当含有低水平c-fgr mRNA的爱泼斯坦-巴尔病毒(EBV)阴性BL细胞系被EBV感染时,c-fgr基因的转录会进一步被诱导。在本文中,我们表明用全反式维甲酸处理EBV阴性和EBV阳性BL细胞系也会刺激c-fgr mRNA水平升高,升高幅度在2至13倍之间,具体取决于细胞系。处理后12至48小时可检测到升高,具体取决于细胞系,这表明c-fgr基因不是直接受维甲酸调控,而是对细胞中其他维甲酸诱导的变化做出反应。我们还表明,用全反式维甲酸处理BL细胞系,要么导致生长速率呈剂量依赖性下降,要么对生长没有影响,具体取决于细胞系。此前有人提出,c-fgr基因产物可能在调节BL细胞生长中起作用,因为用α-干扰素处理EBV阳性BL细胞系Daudi会导致c-fgr mRNA水平下降,随后生长速率降低。我们的数据表明,BL细胞中c-fgr mRNA水平与生长速率之间没有普遍的相关性,因此反对c-fgr基因产物在这些细胞生长调节中起作用的观点。

相似文献

1
Retinoic acid induces changes in c-fgr proto-oncogene mRNA levels in Burkitt's lymphoma cells.维甲酸可诱导伯基特淋巴瘤细胞中c-fgr原癌基因mRNA水平发生变化。
Immunobiology. 1993 Aug;188(4-5):460-8. doi: 10.1016/S0171-2985(11)80227-5.
2
Regulation of c-fgr proto-oncogene expression in Burkitt's lymphoma cells: effect of interferon treatment and relationship to EBV status and c-myc mRNA levels.伯基特淋巴瘤细胞中c-fgr原癌基因表达的调控:干扰素治疗的效果及其与EB病毒状态和c-myc mRNA水平的关系。
Oncogene. 1989 Aug;4(8):1043-6.
3
fgr proto-oncogene mRNA induced in B lymphocytes by Epstein-Barr virus infection.
Nature. 1986;319(6050):238-40. doi: 10.1038/319238a0.
4
Regulation of c-fgr proto-oncogene expression in Epstein-Barr virus infected B-cell lines.
Int J Cancer. 1990 Feb 15;45(2):342-6. doi: 10.1002/ijc.2910450222.
5
Epstein-Barr virus-encoded poly(A)(-) RNA supports Burkitt's lymphoma growth through interleukin-10 induction.爱泼斯坦-巴尔病毒编码的聚腺苷酸(-)RNA通过诱导白细胞介素-10促进伯基特淋巴瘤生长。
EMBO J. 2000 Dec 15;19(24):6742-50. doi: 10.1093/emboj/19.24.6742.
6
Antiimmunoglobulin inhibition of Burkitt's lymphoma cell proliferation and concurrent reduction of c-myc and mu heavy chain gene expression.抗免疫球蛋白对伯基特淋巴瘤细胞增殖的抑制作用以及c-myc和μ重链基因表达的同时降低。
Cancer Res. 1989 Jun 15;49(12):3235-41.
7
Retinoic acid induces persistent, RARalpha-mediated anti-proliferative responses in Epstein-Barr virus-immortalized b lymphoblasts carrying an activated C-MYC oncogene but not in Burkitt's lymphoma cell lines.维甲酸在携带激活型C-MYC癌基因的爱泼斯坦-巴尔病毒永生化B淋巴母细胞中诱导持续的、由维甲酸受体α(RARα)介导的抗增殖反应,但在伯基特淋巴瘤细胞系中则不然。
Int J Cancer. 2000 May 1;86(3):375-84. doi: 10.1002/(sici)1097-0215(20000501)86:3<375::aid-ijc12>3.0.co;2-z.
8
Suppression of the malignant phenotype in somatic cell hybrids between Burkitt's lymphoma cells and Epstein-Barr virus-immortalized lymphoblastoid cells despite deregulated c-myc expression.尽管c-myc表达失调,但伯基特淋巴瘤细胞与爱泼斯坦-巴尔病毒永生化淋巴母细胞样细胞之间的体细胞杂交体中恶性表型受到抑制。
Cancer Res. 1990 May 15;50(10):3095-100.
9
Sensitivity to dexamethasone and absence of bcl-2 protein in Burkitt's lymphoma cell line (Black93) derived from a patient with acute tumor lysis syndrome: comparative study with other BL and non-BL lines.一名急性肿瘤溶解综合征患者来源的伯基特淋巴瘤细胞系(Black93)对地塞米松的敏感性及bcl-2蛋白缺失:与其他伯基特淋巴瘤及非伯基特淋巴瘤细胞系的比较研究
Leukemia. 1996 Oct;10(10):1592-603.
10
Theophylline induced differentiation provides direct evidence for the deregulation of c-myc in Burkitt's lymphoma and suggests participation of immunoglobulin enhancer sequences.茶碱诱导分化为伯基特淋巴瘤中c-myc的失调提供了直接证据,并提示免疫球蛋白增强子序列参与其中。
Cancer Res. 1993 Jan 1;53(1):127-32.

引用本文的文献

1
Kinase inhibitors in cancer therapy: a look ahead.癌症治疗中的激酶抑制剂:展望未来。
Drugs. 2000 Mar;59(3):435-76. doi: 10.2165/00003495-200059030-00004.