Reversible inhibition of normal human prokeratinocyte proliferation by type β transforming growth factor-growth inhibitor in serum-free medium

• Published in: Cancer research (Chicago, Ill.) Vol. 46; no. 4; pp. 2068 - 2071
• Main Authors: SHIPLEY, G. D, PITTELKOW, M. R, WILLE, J. J. JR, SCOTT, R. E, MOSES, H. L
• Format: Journal Article
• Language: English
• Published: Philadelphia, PA American Association for Cancer Research 01.04.1986
• Subjects: Biological and medical sciences; Blood; Carcinoma, Squamous Cell - pathology; Cell Division - drug effects; Cells, Cultured; Culture Media; Epidermis - cytology; Epidermis - drug effects; General aspects (metabolism, cell proliferation, established cell line...); Growth Inhibitors - metabolism; Growth Inhibitors - pharmacology; Humans; Interphase - drug effects; Keratins; Medical sciences; Peptides - metabolism; Peptides - pharmacology; Transforming Growth Factors; Tumor cell; Tumors; Human; Cell proliferation; Cell culture; Growth inhibitor; Squamous cell carcinoma; Conditioned medium; Experimental study; Normal; Membrane receptor; Cell cycle; Keratinocyte; Tumor; Inhibition; Tumor cell
• ISSN: 0008-5472; 1538-7445

Type beta transforming growth factor-growth inhibitor (TGF beta/GI) causes normal human prokeratinocytes to arrest growth predominantly in the G1 phase of the cell cycle within 48 h after log phase cultures are exposed to the factor in serum-free medium. The growth arrest induced by TGF beta/GI is reversible because the cells from treated cultures can be replated into fresh medium and grown into large colonies. Normal prokeratinocytes are demonstrated to secrete TGF beta/GI-like molecules into the culture medium and to have specific cell surface receptors for this molecule. In contrast, a human squamous cell carcinoma, SCC-25, does not arrest growth when exposed to TGF beta/GI. These cells, unlike the normal prokeratinocytes, do not exhibit detectable cell surface receptors for the factor.