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1
Farnesyltransferase inhibitor FTI-277 prevents autocrine growth stimulation of neuroblastoma by BDNF.法尼基转移酶抑制剂FTI-277可阻止脑源性神经营养因子（BDNF）对神经母细胞瘤的自分泌生长刺激。
J Cancer Res Clin Oncol. 2003 Apr;129(4):227-33. doi: 10.1007/s00432-003-0418-x. Epub 2003 Apr 17.
2
Induction of N-myc in neuroblastoma by autocrine IGF-II depends on farnesylated Ras. Application of farnesyltransferase inhibitors.自分泌胰岛素样生长因子-II（IGF-II）诱导神经母细胞瘤中N-myc的表达依赖于法尼基化的Ras。法尼基转移酶抑制剂的应用。
Anticancer Res. 2002 Nov-Dec;22(6C):4205-9.
3
Inhibition of the prenylation of K-Ras, but not H- or N-Ras, is highly resistant to CAAX peptidomimetics and requires both a farnesyltransferase and a geranylgeranyltransferase I inhibitor in human tumor cell lines.抑制K-Ras的异戊二烯化，而非H-Ras或N-Ras的异戊二烯化，对CAAX肽模拟物具有高度抗性，并且在人肿瘤细胞系中需要法尼基转移酶和香叶基香叶基转移酶I抑制剂两者共同作用。
Oncogene. 1997 Sep;15(11):1283-8. doi: 10.1038/sj.onc.1201296.
4
Farnesyltransferase inhibitor (L-744,832) restores TGF-beta type II receptor expression and enhances radiation sensitivity in K-ras mutant pancreatic cancer cell line MIA PaCa-2.法尼基转移酶抑制剂（L-744,832）可恢复转化生长因子-β II型受体表达，并增强K-ras突变型胰腺癌细胞系MIA PaCa-2的辐射敏感性。
Oncogene. 2002 Nov 7;21(51):7883-90. doi: 10.1038/sj.onc.1205948.
5
Both farnesyltransferase and geranylgeranyltransferase I inhibitors are required for inhibition of oncogenic K-Ras prenylation but each alone is sufficient to suppress human tumor growth in nude mouse xenografts.法尼基转移酶抑制剂和香叶基香叶基转移酶I抑制剂对于抑制致癌性K-Ras异戊二烯化都是必需的，但单独使用任何一种都足以抑制裸鼠异种移植瘤中的人类肿瘤生长。
Oncogene. 1998 Mar;16(11):1467-73. doi: 10.1038/sj.onc.1201656.
6
Growth inhibition by the farnesyltransferase inhibitor FTI-277 involves Bcl-2 expression and defective association with Raf-1 in liver cancer cell lines.法尼基转移酶抑制剂FTI-277对肝癌细胞系的生长抑制作用涉及Bcl-2表达以及与Raf-1的结合缺陷。
Mol Pharmacol. 2003 Jan;63(1):159-66. doi: 10.1124/mol.63.1.159.
7
Inhibition of DNA synthesis by a farnesyltransferase inhibitor involves inhibition of the p70(s6k) pathway.
J Biol Chem. 1999 Feb 19;274(8):4743-8. doi: 10.1074/jbc.274.8.4743.
8
The farnesyl transferase inhibitor, FTI-277, inhibits growth and induces apoptosis in drug-resistant myeloma tumor cells.法尼基转移酶抑制剂FTI-277可抑制耐药骨髓瘤肿瘤细胞的生长并诱导其凋亡。
Leukemia. 2003 Feb;17(2):451-7. doi: 10.1038/sj.leu.2402832.
9
Transformation-selective apoptotic program triggered by farnesyltransferase inhibitors requires Bin1.法尼基转移酶抑制剂触发的转化选择性凋亡程序需要Bin1。
Oncogene. 2003 Jun 5;22(23):3578-88. doi: 10.1038/sj.onc.1206481.
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In vitro and in vivo effects of a farnesyltransferase inhibitor on Nf1-deficient hematopoietic cells.法尼基转移酶抑制剂对Nf1缺陷造血细胞的体外和体内作用。
Blood. 1999 Oct 1;94(7):2469-76.

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AP-1 Transcription Factors Mediate BDNF-Positive Feedback Loop in Cortical Neurons.AP-1转录因子介导皮质神经元中的脑源性神经营因子正反馈回路。
J Neurosci. 2016 Jan 27;36(4):1290-305. doi: 10.1523/JNEUROSCI.3360-15.2016.

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Neuroblastoma: inhibition of progression (Part II). Basic science in pediatric surgery.神经母细胞瘤：进展抑制（第二部分）。小儿外科基础科学。
Eur J Pediatr Surg. 2001 Dec;11(6):363-7. doi: 10.1055/s-2001-19725.
2
Current status of clinical trials of farnesyltransferase inhibitors.法尼基转移酶抑制剂的临床试验现状
Curr Opin Oncol. 2001 Nov;13(6):470-6. doi: 10.1097/00001622-200111000-00009.
3
Arglabin-DMA, a plant derived sesquiterpene, inhibits farnesyltransferase.阿格拉宾 - DMA，一种源自植物的倍半萜烯，可抑制法尼基转移酶。
Oncol Rep. 2001 Jan-Feb;8(1):173-9. doi: 10.3892/or.8.1.173.
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SiMa, a new neuroblastoma cell line combining poor prognostic cytogenetic markers with high adrenergic differentiation.
Cancer Genet Cytogenet. 1999 Jul 15;112(2):161-4. doi: 10.1016/s0165-4608(98)00269-6.
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Inhibition of farnesyl-protein-transferase in neuroblastoma cells by alpha-hydroxyfarnesylphosphonate.α-羟基法尼基膦酸酯对神经母细胞瘤细胞中法尼基蛋白转移酶的抑制作用。
Anticancer Res. 1999 Jul-Aug;19(4B):2959-62.
6
N-Myc induction stimulated by insulin-like growth factor I through mitogen-activated protein kinase signaling pathway in human neuroblastoma cells.胰岛素样生长因子I通过丝裂原活化蛋白激酶信号通路刺激人神经母细胞瘤细胞中N-Myc的诱导。
Cancer Res. 2000 Jan 1;60(1):64-9.
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The mouse neurotrophin receptor trkB gene is transcribed from two different promoters.
Biochim Biophys Acta. 1999 Jul 7;1446(1-2):24-34. doi: 10.1016/s0167-4781(99)00056-1.
8
Non-Ras targets of farnesyltransferase inhibitors: focus on Rho.法尼基转移酶抑制剂的非Ras靶点：聚焦于Rho
Oncogene. 1998 Sep 17;17(11 Reviews):1439-45. doi: 10.1038/sj.onc.1202175.
9
Detection of rare target genes on northern blots with cDNA probes labeled by reverse transcriptase-polymerase chain reaction with simultaneous digoxigenin incorporation.
Anal Biochem. 1998 Aug 15;262(1):77-9. doi: 10.1006/abio.1998.2783.
10
Both farnesyltransferase and geranylgeranyltransferase I inhibitors are required for inhibition of oncogenic K-Ras prenylation but each alone is sufficient to suppress human tumor growth in nude mouse xenografts.法尼基转移酶抑制剂和香叶基香叶基转移酶I抑制剂对于抑制致癌性K-Ras异戊二烯化都是必需的，但单独使用任何一种都足以抑制裸鼠异种移植瘤中的人类肿瘤生长。
Oncogene. 1998 Mar;16(11):1467-73. doi: 10.1038/sj.onc.1201656.

法尼基转移酶抑制剂FTI-277可阻止脑源性神经营养因子（BDNF）对神经母细胞瘤的自分泌生长刺激。

Farnesyltransferase inhibitor FTI-277 prevents autocrine growth stimulation of neuroblastoma by BDNF.

作者信息

Girgert Rainer, Wittrock Josefa, Pfister Sabine, Schweizer Paul

机构信息

Department of Gynecology and Obstetrics, University of Ulm, Prittwitzstrasse 43, 89075, Ulm, Germany.

出版信息

J Cancer Res Clin Oncol. 2003 Apr;129(4):227-33. doi: 10.1007/s00432-003-0418-x. Epub 2003 Apr 17.

DOI:10.1007/s00432-003-0418-x
PMID:12700894
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12161948/
Abstract

PURPOSE

Autocrine growth stimulation by IGF-II and BDNF is frequently observed in neuroblastoma. The signals of the receptors of these growth factors are transduced to the nucleus via the Ras-MAP-kinase pathway where they induce proliferation. Inactivation of Ras-proteins by farnesyltransferase inhibitors such as FTI-277 disrupts growth stimulation of ras-transformed cells. We investigated whether FTI-277 is also active against tumor cells with constitutively activated growth factor receptors but lacking ras-mutations.

METHOD

We analyzed eight different neuroblastoma cell lines for the expression of BDNF and its receptor trkB. Two of these cell lines with a complete autocrine BDNF loop were treated with FTI-277, and the effects of Ras-inactivation on the signal transduction of BDNF were analyzed.

RESULTS

Treatment of neuroblastoma cells with 10 microM FTI-277 for 4 days reduced the amount of membrane-bound Ras-protein to almost 50%. Activation of MAP-kinase, induction of N-myc expression, and proliferation were clearly reduced in the treated cells. In addition, we observed some cytotoxic effects of FTI-277 accompanied by morphological changes of the neuroblastoma cells and a delayed induction of apoptosis.

CONCLUSION

Farnesyltransferase inhibitors are active against neuroblastoma cells but the mechanism of action is not limited to inactivation of Ras. Further investigations on the targets of FTI-277 are recommended.

摘要

目的

胰岛素样生长因子-II（IGF-II）和脑源性神经营养因子（BDNF）的自分泌生长刺激在神经母细胞瘤中经常被观察到。这些生长因子受体的信号通过Ras-丝裂原活化蛋白激酶（MAP）途径转导至细胞核，在那里诱导细胞增殖。法尼基转移酶抑制剂如FTI-277使Ras蛋白失活，从而破坏Ras转化细胞的生长刺激。我们研究了FTI-277对具有组成性激活的生长因子受体但缺乏Ras突变的肿瘤细胞是否也有活性。

方法

我们分析了八种不同的神经母细胞瘤细胞系中BDNF及其受体trkB的表达。其中两个具有完整自分泌BDNF环路的细胞系用FTI-277处理，分析Ras失活对BDNF信号转导的影响。

结果

用10微摩尔/升的FTI-277处理神经母细胞瘤细胞4天，使膜结合Ras蛋白的量减少到近50%。处理后的细胞中，MAP激酶的激活、N-myc表达的诱导和细胞增殖明显减少。此外，我们观察到FTI-277有一些细胞毒性作用，伴有神经母细胞瘤细胞的形态变化和凋亡的延迟诱导。

结论

法尼基转移酶抑制剂对神经母细胞瘤细胞有活性，但其作用机制不限于使Ras失活。建议对FTI-277的靶点进行进一步研究。