Extracellular matrix regulates steady-state mRNA levels of the proliferation associated protein Ki-67 in endometrial cancer cells

• Published in: Cancer letters 1999-06, Vol.140 (1), p.145-152
• Main Authors: Tan, Marselina I, Strunck, Elisabeth, Scholzen, Thomas, Gerdes, Johannes, Vollmer, Günter
• Format: Article
• Language: English
• Subjects: Adenocarcinoma - metabolism; Biological and medical sciences; Cell Differentiation - physiology; Cell Division - drug effects; Cell Division - physiology; Collagen - pharmacology; Drug Combinations; Endometrial cancer cells; Endometrial Neoplasms - metabolism; Extracellular matrix; Extracellular Matrix - physiology; Female; Female genital diseases; Gene Expression Regulation - drug effects; Gynecology. Andrology. Obstetrics; Humans; Ki-67 Antigen - genetics; Ki-67 Antigen - metabolism; Laminin - pharmacology; Medical sciences; Peptide Fragments - pharmacology; Protein Ki-67; Proteoglycans - pharmacology; RNA, Messenger - metabolism; Steady-state mRNA; Tenascin - pharmacology; Tumor Cells, Cultured; Tumors
• ISSN: 0304-3835; 1872-7980
• DOI: 10.1016/S0304-3835(99)00066-X

We investigated whether components of the extracellular matrix have the potential to regulate the proliferative activity of endometrial adenocarcinoma cells. Culturing of cells on the reconstituted basement membrane matrigel™ down-regulated the steady-state mRNA levels of the proliferation associated protein, Ki-67, in the endometrial adenocarcinoma cell lines HEC 1B(L) and Ishikawa after 48–96 h of culture on the matrix substrate. Proliferation of Ishikawa was stimulated again if cells were cultured on matrigel and challenged by proteins representing functional domains of tenascin-C, a mesenchymal glycoprotein. The fibronectin-type-III-like repeats 6–8 of tenascin-C were found to be the most potent. In summary, evidence is provided that components of both epithelial and stromal extracellular matrices can function as regulators of cell growth.