Evaluation of Biologic Phenotype by Midkine Gene Expression in Gastric Cancer as a Target for Biotherapy.
- Author:
Hyun Cheol CHUNG
1
;
Sun Young RHA
;
Hei Cheol CHUNG
;
Hyun Joo KWAK
;
Jae Yong CHO
;
Soo Jung GONG
;
Sung Hoon NOH
;
Joo Hang KIM
;
Jae Kyung ROH
;
Jin Sik MIN
;
Byung Soo KIM
Author Information
1. Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, Korea.
- Publication Type:In Vitro ; Original Article
- Keywords:
Gastric cancer;
Midkine;
Pentosan polysulfate;
Biotherapy
- MeSH:
Agar;
Biological Therapy*;
Blotting, Northern;
Carcinogenesis;
Cell Line;
Endothelial Cells;
Enzyme-Linked Immunosorbent Assay;
Gene Expression*;
Pentosan Sulfuric Polyester;
Phenotype*;
Plasminogen Activator Inhibitor 1;
Stomach Neoplasms*;
Urokinase-Type Plasminogen Activator
- From:Journal of the Korean Cancer Association
1997;29(1):69-80
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: We studied biological phenotypes of gastric cancer cell lines based on a novel heparin-binding growth/differentiation factor, midkine (MK) expression. MATERIALS AND METHODS: Nine gastric cancer cell lines and 25 gastric cancer tissues were tested for MK expression by Northern blot analysis. Soft agar assay for in vitro tumorigenesis, cross- feeding assay for paracrine angiogenic activity, ELISA for uPA and PAI-1 measurement were performed. RESULTS: MK expression was found in 67% (6/9) of the gastric cancer cell lines, and 56% (14/25) of the primary gastric cancer tissues. Gastric cancer cell lines with MK expression were more tumorigenic in soft agar assay and endothelial cell growth stimulatory in cross-feeding assay than cells which did not express MK. However, urokinase-type plasminogen activator (uPA) expression 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. CONCLUSION: Gastric cancer cells with increased MK gene expression showed increased tumorigenic and angiogenic activity. Therefore, this proliferation promoting activity of MK can be targeted by an anti-heparin binding agent as a biotherapy model in gastric cancer treatment.
