排序方式： 共有44条查询结果，搜索用时 15 毫秒
11.
AIM: To investigate the effect of Eph receptor A2 (EphA2) on drug resistance of colorectal carcinoma cells and its possible mechanisms. METHODS: Real-time PCR and Western blot were used to detect the expression of EphA2 at mRNA and protein levels in LoVo and LoVo/5-FU cells. EphA2 siRNA was transfected to down-regulate the EphA2 expression in LoVo/5-FU cells, and the drug sensitivity was calculated by CCK-8 assay. Meanwhile, cell migration and invasion were measured by wound healing assay and Transwell assay, and the protein levels of E-cadherin, β-catenin, N-cadherin, vimentin, Notch and Snail were determined by Western blot. RESULTS: The expression of EphA2 at both mRNA and protein levels was significantly up-regulated in LoVo/5-FU cells (P<0.05). Knockdown of EphA2 suppressed the cell viability, and migration and invasion abilities, but promoted drug sensitivity of LoVo/5-FU cells. Up-regulation of E-cadherin and β-catenin, and down-regulation of N-cadherin and vimentin were observed, indicating that the epithelial-mesenchymal transition (EMT) process was suppressed. Knockdown of EphA2 decreased the expression levels of Notch and Snail. CONCLUSION: Down-regulation of EphA2 partly reverses drug resistance of LoVo/5-FU cells. The mechanism may be related to suppressing cell growth, migration, invasion and EMT process via Notch/Snail signaling pathway. 相似文献
12.
13.
骨骼系统对机体的生命活动至关重要，它为生物体提供了造血微环境、机械支撑、保护脏器等功能，同时也是钙和其他矿物质等的储存库。家鸡尾骨的表型多样性是研究骨骼系统发育及形成机制的良好资源。Notch、Wnt信号通路的靶基因及其相互作用可以形成周期性表达的特点，是调节体节形成及尾部骨骼终止延伸的分子通路。为了解无尾鸡骨骼发育终止的分子机制，作者分别总结了骨骼发育、无尾鸡骨骼研究进展，并重点讨论影响无尾性状的关键信号通路Notch、Wnt及其在无尾鸡研究中的进展。但是，受体和配体之间相互作用的精确调节以及信号通路中的核心元素仍不清楚，需要通过更多的功能基因组和蛋白质组等方法进行深入研究。 相似文献
14.
15.
16.
17.
AIM: To investigate the effect of Notch1 gene silencing on phosphorylations of JNK1 and p53 in human breast cancer MCF-7 cells.METHODS: shRNA-Notch1 eukaryotic expression plasmid was constructed and transfected into MCF-7 cells. The expression of Notch1 and Hes-1 was observed by Western blotting after transfction. Apoptosis and mitochondrial membrane potential were detected by flow cytometry. Western blotting was also used to determine the protein levels of p-JNK1, p-p53, PUMA, NOXA and cleaved caspase-3 after Notch1 silencing was performed in MCF-7 cells.RESULTS: Silencing of Notch1 significantly reduced the expression of Notch1 and Hes-1 in MCF-7 cells (P<0.01). In shNotch1 group, the number of apoptotic cells was much higher (P<0.01) and mitochondrial membrane potential was much lower (P<0.05) than those in shControl group. The protein levels of p-JNK1, p-p53, PUMA, NOXA and cleaved caspase-3 increased obviously after silencing of Notch1 was performed in MCF-7 cells (P<0.05).CONCLUSION: Notch1 silencing induces apoptosis of human breast cancer MCF-7 cells through promoting phosphorylations of JNK1 and p53, and increasing the production of PUMA, NOXA and cleaved caspase-3. 相似文献
18.
AIM: To investigate the proliferation and migration of neural stem cells (NSCs) in the subventricular zone (SVZ) on focal cerebral ischemia with curcumin treatment, and to explore the relationship between these effects and Notch signaling. METHODS: The animal model was established by an intraluminal suture method to induce middle cerebral artery occlusion in rats. The rats were randomly divided into sham group, cerebral ischemia/reperfusion (I/R) group, and I/R+curcumin group. The animals were given curcumin for 7 d intraperitoneally. One hour after the model was successfully established, the rats were sacrificed. Immunofluorescence was used to label the NSCs by BrdU and BrdU/DCX, and the migration tendency was observed. The expression of Notch intracellular domain (NICD, the Notch signaling pathway intermediate product) was detected by Western blotting. RESULTS: Compared with I/R group, BrdU-positive and BrdU/DCX double positive cells in I/R+curcumin group were significantly higher than those in I/R group (P<0.05), and more positive cells were on the way of migration to the ischemic lesion zone. The expression level of NICD in I/R+curcumin group was significantly higher than that in I/R group (P<0.05). CONCLUSION: Curcumin promotes NSC proliferation and migration in SVZ after focal cerebral ischemia. The possible mechanism may be that curcumin activates Notch signaling. 相似文献
19.
20.