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Comparison of biological phenotypes according to midkine expression in gastric cancer cells and their autocrine activities could be modulated by pentosan polysulfate

Authors
 Sun Young Rha  ;  Sung Hoon Noh  ;  Hyun Joo Kwak  ;  Anton Wellstein  ;  Joo Hang Kim  ;  Jae Kyung Roh  ;  Jin Sik Min  ;  Byung Soo Kim  ;  Hyun Cheol Chung 
Citation
 CANCER LETTERS, Vol.118(1) : 37-46, 1997 
Journal Title
 CANCER LETTERS 
ISSN
 0304-3835 
Issue Date
1997
MeSH
Ascitic Fluid ; Carrier Proteins/biosynthesis* ; Cell Differentiation ; Cell Division/drug effects ; Cytokines/biosynthesis* ; Endothelial Growth Factors/biosynthesis ; Humans ; Lymphokines/biosynthesis ; Midkine ; Neoplasm Staging ; Neovascularization, Pathologic ; Pentosan Sulfuric Polyester/pharmacology* ; Phenotype ; Plasminogen Activator Inhibitor 1/biosynthesis ; RNA, Messenger/biosynthesis ; Stomach Neoplasms/genetics ; Stomach Neoplasms/metabolism* ; Stomach Neoplasms/pathology* ; Tumor Cells, Cultured ; Tumor Stem Cell Assay ; Urokinase-Type Plasminogen Activator/biosynthesis ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
Abstract
We studied biological phenotypes of gastric cancer cell lines based on a novel heparin-binding growth/differentiation factor (midkine (MK)) expression. MK expression was found in 67% (6/9) of the gastric cancer cell lines and 56% (14/25) of the primary cancer tissues. Gastric cancer cell lines with MK expression showed higher colony forming activity in soft agar assay and endothelial cell growth stimulatory effect in cross-feeding assay than cells which did not express MK. However, urokinase-type plasminogen activator (uPA) expression and tumor invasiveness did not correlate with MK expression. Growth of MK expressing cells was inhibited by a heparin-binding blocking agent, pentosan polysulfate (PPS). In cancer tissues, MK expression correlated with tumor size, suggesting in vivo autocrine and paracrine activity. This proliferation promoting activity of MK can be targeted by an anti-heparin binding agent as a biotherapy model in gastric cancer.
Full Text
https://www.sciencedirect.com/science/article/pii/S0304383597002152?via%3Dihub
DOI
10.1016/s0304-3835(97)00215-2
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Surgery (외과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Joo Hang(김주항)
Noh, Sung Hoon(노성훈) ORCID logo https://orcid.org/0000-0003-4386-6886
Roh, Jae Kyung(노재경)
Rha, Sun Young(라선영) ORCID logo https://orcid.org/0000-0002-2512-4531
Chung, Hyun Cheol(정현철) ORCID logo https://orcid.org/0000-0002-0920-9471
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/177279
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