KAI1 reverses the epithelial-mesenchymal transition in human pancreatic cancer cells
查看参考文献34篇
文摘
|
Background: 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. |
来源
|
Hepatobiliary & Pancreatic Diseases International
,2019,18(5):471-477 【核心库】
|
DOI
|
10.1016/j.hbpd.2019.03.004
|
关键词
|
KAI1
;
Epithelial-mesenchymal transition
;
Pancreatic cancer
|
地址
|
Department of Gastroenterology, General Hospital of Shenyang Military Area, Shenyang, 110840
|
语种
|
英文 |
文献类型
|
研究性论文 |
ISSN
|
1499-3872 |
学科
|
肿瘤学 |
基金
|
国家自然科学基金
;
the Science Foundation of Liaoning
|
文献收藏号
|
CSCD:6604826
|
参考文献 共
34
共2页
|
1.
Mcguire S.
World cancer report 2014. Geneva, Switzerland: world health organization, international agency for research on cancer,2015
|
被引
4
次
|
|
|
|
2.
Mcguire S.
Adv Nutr,2016,7:418-419
|
被引
85
次
|
|
|
|
3.
Ferlay J. Cancer incidence and mortality worldwide: sources, methods and major patterns in GLOBOCAN 2012.
Int J Cancer,2015,136:E359–E386
|
被引
1093
次
|
|
|
|
4.
Lamouille S. Molecular mechanisms of epithelial-mesenchymal transition.
Nat Rev Mol Cell Biol,2014,15:178-196
|
被引
258
次
|
|
|
|
5.
Stone R C. Epithelial-mesenchymal transition in tissue repair and fibrosis.
Cell Tissue Res,2016,365:495-506
|
被引
27
次
|
|
|
|
6.
Jie X X. Epithelial-to-mesenchymal transition, circulating tumor cells and cancer metastasis: mechanisms and clinical applications.
Oncotarget,2017,8:81558-81571
|
被引
11
次
|
|
|
|
7.
Krantz S B. Contribution of epithelial-to-mesenchymal transition and cancer stem cells to pancreatic cancer progression.
J Surg Res,2012,173:105-112
|
被引
9
次
|
|
|
|
8.
Gaianigo N. EMT and treatment resistance in pancreatic cancer.
Cancers (Basel),2017,9:122
|
被引
3
次
|
|
|
|
9.
Beuran M. The epithelial to mesenchymal transition in pancreatic cancer: a systematic review.
Pancreatology,2015,15:217-225
|
被引
8
次
|
|
|
|
10.
Gonzalez D M. Signaling mechanisms of the epithelial-mesenchymal transition.
Sci Signal,2014,7:re8
|
被引
57
次
|
|
|
|
11.
Huang W. Expression of PTEN and KAI1 tumor suppressor genes in pancreatic carcinoma and its association with different pathological factors.
Oncol Lett,2016,11:559-562
|
被引
1
次
|
|
|
|
12.
Miranti C K. Controlling cell surface dynamics and signaling: how CD82/KAI1 suppresses metastasis.
Cell Signal,2009,21:196-211
|
被引
9
次
|
|
|
|
13.
Liu X. KAI1 inhibits lymphangiogenesis and lymphatic metastasis of pancreatic cancer in vivo.
Hepatobiliary Pancreat Dis Int,2014,13:87-92
|
被引
2
次
|
|
|
|
14.
Prieto-Garcia E. Epithelial-to-mesenchymal transition in tumor progression.
Med Oncol,2017,34:122
|
被引
10
次
|
|
|
|
15.
Liu X. KAI1 inhibits HGF-induced invasion of pancreatic cancer by sphingosine kinase activity.
Hepatobiliary Pancreat Dis Int,2011,10:201-208
|
被引
4
次
|
|
|
|
16.
Liu X. Src/STAT3 signaling pathways are involved in KAI1-induced downregulation of VEGF-C expression in pancreatic cancer.
Mol Med Rep,2016,13:4774-4778
|
被引
5
次
|
|
|
|
17.
Wu C Y. Overexpression of KAI1 induces autophagy and increases MiaPaCa-2 cell survival through the phosphorylation of extracellular signal-regulated kinases.
Biochem Biophys Res Commun,2011,404:802-808
|
被引
3
次
|
|
|
|
18.
Wu C Y. Hypoxia and serum deprivation protected MiaPaCa-2 cells from KAI1-induced proliferation inhibition through autophagy pathway activation in solid tumors.
Clin Transl Oncol,2015,17:201-208
|
被引
2
次
|
|
|
|
19.
Cano C E. Epithelial-to-mesenchymal transition in pancreatic adenocarcinoma.
Scientific World J,2010,10:1947-1957
|
被引
7
次
|
|
|
|
20.
Liu X. E-cadherin and gastric cancer: cause, consequence, and applications.
Biomed Res Int,2014,2014:637308
|
被引
5
次
|
|
|
|
|