Epithelial mesenchymal transition correlates with CD24+CD44+ and CD133+             cells in pancreatic cancer.
The epithelial-mesenchymal transition (EMT) has been linked to induction             of a stem-cell like phenotype, characterized by altered cell surface marker expression             and increased tumor formation. The aim of this study was to investigate whether             EMT correlates with CD24+CD44+ and CD133+ cells in pancreatic cancer. The morphology             of untreated and gemcitabine-treated SW1990 gemcitabine-resistant cells and normal             SW1990 cells were compared. NF-κB p65 expression was knocked down using siRNA.             Vimentin and E-cadherin expression were analyzed using western blotting, and CD24+CD44+,             CD133+ cells were quantified by FACS. Additionally, immunohistochemistry of EMT-associated             markers and stem cell-associated markers were performed in 41 cases of human pancreatic             ductal adenocarcinoma. In SW1990 gemcitabine-resistant cells, gemcitabine induced             a mesenchymal cell phenotype, expression of EMT-related molecular markers and             increased CD24+CD44+ and CD133+ cells compared to untreated SW1990 gemcitabine-resistant             and SW1990 cells. Knockdown of NF-κB p65 inhibited the ability of gemcitabine             to increase the proportion of CD24+CD44+ or CD133+ cells and expression of EMT-related             molecular markers. In human pancreatic ductal adenocarcinoma, significant correlations             were observed between expression of the EMT-associated markers vimentin and E-cadherin,             and stem cell-associated markers CD24, CD133 and CD44. This study demonstrated             that EMT correlated with CD24+CD44+ and CD133+ cells in pancreatic cancer. This             study also suggests that EMT may induce cancer stem-like cells in pancreatic cancer,             with different degrees of EMT probability inducing different proportions of CD24+CD44+             and CD133+ cells.
Department of Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, PR China.
Ye
Y
Zhang
Jishu
J
Wei
Hui
H
Wang
Xiaofeng
X
Xue
Yong
Y
An
Dong
D
Tang
Zhongxu
Z
Yuan
Feitong
F
Wang
Junli
J
Wu
Jingjing
J
Zhang
Yi
Y
Miao
D000071916:AC133 Antigen; D015703:Antigens, CD / Q000235:genetics / Q000378:metabolism*; D017209:Apoptosis / Q000235:genetics; D051927:CD24 Antigen / Q000235:genetics / Q000378:metabolism*; D015820:Cadherins / Q000378:metabolism; D021441:Carcinoma, Pancreatic Ductal / Q000235:genetics / Q000378:metabolism*; D045744:Cell Line, Tumor; D058750:Epithelial-Mesenchymal Transition / Q000235:genetics; D020868:Gene Silencing; D006023:Glycoproteins / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D018960:Hyaluronan Receptors / Q000235:genetics / Q000378:metabolism*; D016130:Immunophenotyping; D009361:Neoplasm Invasiveness / Q000235:genetics; D010190:Pancreatic Neoplasms / Q000235:genetics / Q000378:metabolism*; D010455:Peptides / Q000235:genetics / Q000378:metabolism*; D010641:Phenotype; D034741:RNA, Small Interfering / Q000378:metabolism; D051996:Transcription Factor RelA / Q000235:genetics / Q000378:metabolism
D000071916:AC133 Antigen; D015703:Antigens, CD; D051927:CD24 Antigen; D015820:Cadherins; D006023:Glycoproteins; D018960:Hyaluronan Receptors; C000606023:PROM1 protein, human; D010455:Peptides; D034741:RNA, Small Interfering; D051996:Transcription Factor RelA