Activation of the PI3K/Akt Pathway Mediates Bone Morphogenetic Protein 2-Induced Invasion of Pancreatic Cancer Cells Panc-1
Activation of the PI3K/Akt Pathway Mediates Bone Morphogenetic Protein 2-Induced Invasion of Pancreatic Cancer Cells Panc-1
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DOI：
10.1007/s12253-010-9307-1
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发表时间：
2011-06-01
影响因子：
2.8
通讯作者：
Sun, WeiJia
中科院分区：
文献类型：
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作者：
Chen, Xiong;Liao, Jie;Sun, WeiJia
骨形态发生蛋白（BMPs）信号在胰腺癌中的作用正在显现。然而，由于不同的BMP的多种作用，没有最终的结论已作出BMP在胰腺癌中的作用。在我们的研究中，我们专注于骨形态发生蛋白2（BMP-2），因为它诱导上皮间质转化（EMT），并加速人胰腺癌细胞系Panc-1的侵袭。已有报道，磷脂酰肌醇3-激酶（PI 3 K）/Akt通路介导胃癌和结肠癌细胞的侵袭，这在胰腺癌细胞中未被揭示。本研究的目的是研究BMP-2介导的侵袭是否可能通过PI 3 K/Akt通路。我们的研究结果表明，磷酸化Akt的表达增加与BMP-2的治疗，但不是头蛋白，BMP-2拮抗剂。PI 3 K/AKT通路抑制剂LY 294002预处理Panc-1细胞，可显著抑制BMP-2诱导的EMT和侵袭力。这些数据表明，BMP-2通过panc-1细胞中的PI 3 K/AKT通路加速panc-1细胞的侵袭，这为寻找晚期胰腺癌的新治疗靶点提供了线索。
Bone morphogenetic proteins (BMPs) signaling has an emerging role in pancreatic cancer. However, because of the multiple effects of different BMPs, no final conclusions have been made as to the role of BMPs in pancreatic cancer. In our studies, we have focused on bone morphogenetic protein 2(BMP-2) because it induces an epithelial to mesenchymal transition (EMT) and accelerates invasion in the human pancreatic cancer cell line Panc-1. It has been reported that the phosphatidylinositol 3-kinase (PI3K)/Akt pathway mediates invasion of gastric and colon cancer cells, which is unrevealed in pancreatic cancer cells. The objective of our study was to investigate whether BMP-2 mediated invasion might pass through the PI3K/Akt pathway. Our results show that expression of phosphorylation of Akt was increased by treatment with BMP-2, but not Noggin, a BMP-2 antagonist. Then pretreatment of Panc-1 cells with LY294002, an inhibitor of the PI3K/AKT pathway, significantly inhibited BMP-2-induced EMT and invasiveness. The data suggest that BMP-2 accelerates invasion of panc-1 cells via the PI3K/AKT pathway in panc-1 cells, which gives clues to searching new therapy targets in advanced pancreatic cancer.