Different regulation of vascular endothelial growth factor expression by the ERK and p38 kinase pathways in v-ras, v-raf, and v-myc transformed cells.
Different regulation of vascular endothelial growth factor expression by the ERK and p38 kinase pathways in v-ras, v-raf, and v-myc transformed cells.
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v-ras、v-raf 和 v-myc 转化细胞中 ERK 和 p38 激酶途径对血管内皮生长因子表达的不同调节。
DOI：
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发表时间：
2000
期刊：
影响因子：
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通讯作者：
U. Thorgeirsson
中科院分区：
文献类型：
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作者：
Eijiro Okajima;U. Thorgeirsson
在这里，我们表明，血管内皮生长因子（VEGF）mRNA表达上调癌基因转化大鼠肝上皮（RLE）细胞系和细胞外信号调节激酶（ERK）和p38激酶差异调节癌基因介导的刺激VEGF。VEGFmRNA的表达水平在v-H-ras转化的RLE细胞系中最高，其次是v-raf和v-myc转化的细胞系。PD 98059 MEK抑制剂用于阻断ERK通路，SB 203580抑制剂用于阻断p38通路。亲本和v-H-ras转化的RLE细胞系显示通过ERK途径上调VEGF RNA表达，通过p38途径下调VEGF。VEGF在人乳腺癌细胞系中以类似的方式调节。在v-raf和v-myc转化的RLE系中，VEGF的正调节通过p38途径转导。这些发现表明：（1）致癌ras与raf和myc在招募MAPK信号通路调节VEGF方面不同;（2）在ras转化的人癌细胞系和人癌细胞系中，ERK和p38信号通路以阳性和阴性方式调节VEGF。
Here we show that vascular endothelial growth factor (VEGF) mRNA expression is up-regulated in oncogene transformed rat liver epithelial (RLE) cell lines and that the extracellular signal-regulated kinase (ERK) and p38 kinase differentially regulate the oncogene-mediated stimulation of VEGF. The highest level of VEGF mRNA expression was observed in the v-H-ras transformed RLE cell line, followed by the v-raf and v-myc transformed lines. The PD98059 MEK inhibitor was used to block the ERK pathway and SB203580 inhibitor to block the p38 pathway. The parent and the v-H-ras transformed RLE cell lines showed up-regulation of VEGF RNA expression through the ERK pathway and down-regulation of VEGF through the p38 pathway. VEGF was regulated in a comparable manner in a human breast carcinoma cell line. In the v-raf and v-myc transformed RLE lines, positive regulation of VEGF was transduced through the p38 pathway. These findings suggest that (1) oncogenic ras differs from raf and myc in the recruitment of the MAPK signaling pathways for VEGF regulation; (2) that VEGF is regulated in ras transformed and human cancer cell lines in a positive and negative manner by the ERK and p38 signaling pathways.
影响因子：
11.2
作者：
J. Rak;Y. Mitsuhashi;L. Bayko;J. Filmus;S. Shirasawa;T. Sasazuki;R. Kerbel
通讯作者：
J. Rak;Y. Mitsuhashi;L. Bayko;J. Filmus;S. Shirasawa;T. Sasazuki;R. Kerbel