JAK2/STAT3信号通路对胃癌血管生成的影响

傅军; 傅玉春; 张晓雲; 刘春祥; 李路佳; 朱冰

doi:10.13898/j.cnki.issn.1000-2200.2019.06.001

JAK2/STAT3信号通路对胃癌血管生成的影响

Effect of JAK2/STAT3 signaling pathway on the angiogenesis of gastric cancer

摘要

摘要:
目的探讨酪氨酸激酶2/信号转导和转录激活因子3（JAK2/STAT3）信号通路对胃癌血管生成的影响。
方法选择胃癌根治术病人30例，收集胃癌组织、癌旁组织以及正常组织，体外检测JAK2/STAT3信号通路对细胞自噬以及细胞活力的影响，以及自噬蛋白对胃癌细胞分泌血管生成因子的影响。
结果胃癌组织中pJAK2、pSTAT3表达水平高于癌旁组织及正常组织；加入JAK2/STAT3信号通路阻滞剂后，胃癌细胞自噬能力、细胞活力明显减弱（P < 0.01）；过表达自噬蛋白Beclin-1后胃癌细胞分泌血管内皮生长因子（VEGF）和血小板衍化生长因子（PDGF）水平明显高于抑制组（P < 0.01）；而过表达自噬蛋白LC3后，VEGF、PDGF水平与抑制组差异无统计学意义（P>0.05）。
结论JAK2/STAT3信号通路通过调控细胞自噬影响胃癌微血管生成能力，可能是通过激活Beclin-1提高VEGF、PDGF的表达水平。

Abstract:
ObjectiveTo investigate the effects of JAK2/STAT3 signaling pathway on the angiogenesis of gastric cancer.
MethodsThe gastric cancer tissue, pericarcinomatous tissue and normal tissue from 30 patients treated with radical gastrectomy were collected.The effects of JAK2/STAT3 signaling pathway on autophagy and cell viability, and effects of autophagy proteins on the secretion of angiogenic factors in gastric cancer cells were investigated in vitro.
ResultsThe expression levels of pJAK2 and pSTAT3 in gastric cancer tissue were higher than those in pericarcinomatous tissue and normal tissue.The autophagy abilities and cell viabilities of gastric cancer cells significantly decreased after the JAK2/STAT3 signaling pathway was inhibited(P < 0.01).After Beclin-1 was overexpressed, the expression levels of VEGF and PDGF secreted by gastric cancer cells were significantly higher than those in inhibition group(P < 0.01).After the autophagy protein LC3 was overexpressed, the expression levels of VEGF and PDGF between two groups were not statistically significant(P>0.05).
ConclusionsJAK2/STAT3 signaling pathway can affect the microangiogenic ability of gastric cancer cells by regulating the autophagy ability, which maybe increase the expression levels of VEGF and PDGF by activating beclin-1.

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