Naringenin decreases invasiveness and metastasis by inhibiting TGF-β-induced epithelial to mesenchymal transition in pancreatic cancer cells.
Naringenin decreases invasiveness and metastasis by inhibiting TGF-β-induced epithelial to mesenchymal transition in pancreatic cancer cells.
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DOI：
10.1371/journal.pone.0050956
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发表时间：
2012
期刊：
影响因子：
3.7
通讯作者：
Liang W
中科院分区：
文献类型：
--
作者：
Lou C;Zhang F;Yang M;Zhao J;Zeng W;Fang X;Zhang Y;Zhang C;Liang W
上皮向间充质转化(EMT)在胚胎发育和肿瘤发生过程中促进细胞的运动、侵袭和转移。转化生长因子-β(转化生长因子-β)信号通路是子宫内膜间质转化的关键调控因子。大量证据表明，这一过程是Smad3依赖的。在此，我们发现转化生长因子-β-1作用于人胰腺癌细胞ASPC-1和PANC-1后，细胞的形态发生了特征性的改变，细胞的运动能力和对吉西他滨(GEM)的耐受性增强，并上调了EMT标志物基因如波形蛋白、N-钙粘蛋白、基质金属蛋白酶2和基质金属蛋白酶9的表达。通过抑制转化生长因子-Smad1/Smad3信号通路，柚皮素(Nar)下调胰腺癌细胞β-Smad1/Smad3信号通路的表达。因此，NAR抑制了细胞的迁移和侵袭，逆转了细胞对Gem的抗性。
Epithelial to mesenchymal transition (EMT) promotes cellular motility, invasiveness and metastasis during embryonic development and tumorigenesis. Transforming growth factor-β (TGF-β) signaling pathway is a key regulator of EMT. A lot of evidences suggest that this process is Smad3-dependent. Herein we showed that exposure of aspc-1 and panc-1 pancreatic cancer cells to TGF-β1 resulted in characteristic morphological alterations of EMT, and enhancement of cell motility and gemcitabine (Gem) resistance along with an up-regulation of EMT markers genes such as vimentin, N-cadherin, MMP2 and MMP9. Naringenin (Nar) down-regulated EMT markers expression in both mRNA and protein levels by inhibiting TGF-β1/Smad3 signal pathway in the pancreatic cancer cells. Consequently, Nar suppressed the cells migration and invasion and reversed their resistance to Gem.
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