血管生成素通过ERK信号通路促进HeLa细胞的增殖

目的通过细胞外信号调节激酶（extracellularregulatedproteinkinases，ERK）通路及NF-xB信号途径探讨血管生成素（angiogenin，Ang）对HeLa细胞的促增殖及抗凋亡作用机制。方法用不同浓度的重组人Ang刺激HeLa细胞，MTr法分析Ang对HeLa细胞的促增殖作用，蛋白质印迹实验检测ERK信号通路相关分子的表达情况。U0126抑制ERK信号通路，检测Ang诱导的ERKl／2的磷酸化及c—myc的表达情况，同时检测Ang对细胞增殖的影响。敲低Ang的表达，检测细胞的凋亡情况。双荧光素酶报告基因检测Ang对NF-KB报告基因的激活。蛋白水平检测Ang刺激的HeLa细胞后，NF—KB通路相关分子的表达。结果Ang能促进HeLa细胞增殖，ERKl／2的磷酸化水平及c—myc的表达随重组人Ang浓度的升高而增加。U0126能抑制Ang诱导的ERKI／2的磷酸化、c—myc的上调及细胞的增殖。Ang的低表达促进HeLa细胞的凋亡，但不影响NF-KB报告基因的激活及NF—KB通路上相关分子的表达。结论Ang能够促进HeLa细胞增殖，并通过活化ERK通路促进细胞的增殖，但其抑凋亡作用与NF-KB通路无关。

Angiogenin promotes HeLa cell proliferation by activating ERK signaling pathway

Objective To explore the mechanisms for the proliferation-promoting and anti-apoptotic effects of angioge- nin（Ang） on HeLa cells by ERK and NF-KB signaling pathways. Methods Recombinant human Ang（rhAng） of different concentrations was used to stimulate HeLa cells, MTI method to analyze the proliferation-promoting effect of Ang on HeLa cells, and Western blotting to evaluate the expression of the ERK signaling pathway-related molecules. Ang expression was knocked-down and the cell apoptosis was detected. Dual-fluorescent reporter genes were used to detect the activation of NF-KB reporter gene by Ang. The expression of NF-KB signaling pathway-related molecules at the protein level was detec- ted after the stimulation of HeLa cells by Ang. U0126 was used to inhibit ERK signaling pathway, and the Ang-induced ERK1/2 phosphorylation, c-myc expression and cell proliferation were also detected. Results Ang could promote HeLa cell proliferation while the low expression of Ang could promote HeLa cell apoptosis. The level of ERK1/2 phosphorylation and c-myc expression increased with the rhAng concentration, but the activation of NF-KB reporter genes and the expression of NF-KB signaling pathway-related molecules remained unchanged. U0126 could inhibit the Ang-induced ERK1/2 phos- phorylation, up-regulation of c-myc and cell proliferation. Conclusions Ang can promote HeLa cell proliferation and in- hibit cell apoptosis by activating ERK signaling pathway and up-regulating c-myc expression.