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KAI1 reverses the epithelial-mesenchymal transition in human pancreatic cancer cells
Alternative TitleKAI1 reverses the epithelial-mesenchymal transition in human pancreatic cancer cells
Liu Xu; Guo XiaoZhong; Li HongYu; Chen Jiang
2019
Source PublicationHEPATOBILIARY & PANCREATIC DISEASES INTERNATIONAL
ISSN1499-3872
Volume18Issue:5Pages:471-477
AbstractBackground: Epithelial-mesenchymal transition (EMT) plays an important role in pancreatic cancer (PC). In the present study, we investigated the effects of KAI1 gene overexpression on the EMT of human PC cell lines, MIA PaCa-2 and PACN-1.
Other AbstractBackground: Epithelial-mesenchymal transition (EMT) plays an important role in pancreatic cancer (PC). In the present study, we investigated the effects of KAI1 gene overexpression on the EMT of human PC cell lines, MIA PaCa-2 and PACN-1. Methods: Plasmids overexpressing KAI1 and pCMV were transfected into MIA PaCa-2 and PACN-1 cells, respectively. After selection of differently transfected cells by G418, KAI1 protein levels were examined by Western blotting, and transfected cells were renamed as MIA PaCa-2-K, MIA PaCa-2-p, PACN-1-K and PACN-1-p. Wound healing and Transwell migration assays were then performed comparing the two groups of cells. EMT-related markers were analyzed by Western blotting. Results: The percentage of wound closure significantly decreased in MIA PaCa-2-K cells compared with MIA PaCa-2-p and MIA PaCa-2 cells after 24, 48 and 72 h (P < 0.05). In PACN-1-K cells, the percentage of wound closure significantly decreased as well (P < 0.05). Numbers of invading MIA PaCa-2, MIA PaCa-2-p and MIA PaCa-2-K cells were determined as 48.0 ±15.4, 50.0 ±12.4, and 12.0 ±3.8, respectively. The corresponding numbers of invading PACN-1, PACN-1-p and PACN-1-K cells were 29.0 ±10.6, 31.0 ±11.4, and 8.0 ±4.2, respectively. KAI1 overexpression induced a significant upregulation of E-cadherin and also significant downregulation of Snail, vimentin, matrix metalloproteinase 2 (MMP2) and MMP9 (all P < 0.05) in PC cells. Conclusions: KAI1 reversed EMT-related marker expression and inhibited migration and invasion of PC cells. Thus, KAI1 might represent a novel potential therapeutic target for PC.
KeywordEXPRESSION METASTASIS ACTIVATION VIMENTIN ADHESION SNAIL KAI1 Epithelial-mesenchymal transition Pancreatic cancer
Indexed ByCSCD
Language英语
Funding Project[National Natural Science Foundation of China] ; [Science Foundation of Liaoning]
CSCD IDCSCD:6604826
Citation statistics
Cited Times:1[CSCD]   [CSCD Record]
Document Type期刊论文
Identifierhttp://ir.imr.ac.cn/handle/321006/157688
Collection中国科学院金属研究所
Affiliation中国科学院金属研究所
Recommended Citation
GB/T 7714
Liu Xu,Guo XiaoZhong,Li HongYu,et al. KAI1 reverses the epithelial-mesenchymal transition in human pancreatic cancer cells[J]. HEPATOBILIARY & PANCREATIC DISEASES INTERNATIONAL,2019,18(5):471-477.
APA Liu Xu,Guo XiaoZhong,Li HongYu,&Chen Jiang.(2019).KAI1 reverses the epithelial-mesenchymal transition in human pancreatic cancer cells.HEPATOBILIARY & PANCREATIC DISEASES INTERNATIONAL,18(5),471-477.
MLA Liu Xu,et al."KAI1 reverses the epithelial-mesenchymal transition in human pancreatic cancer cells".HEPATOBILIARY & PANCREATIC DISEASES INTERNATIONAL 18.5(2019):471-477.
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