AUTOCRINE GROWTH-MECHANISM BY TRANSFORMING GROWTH-FACTOR (TGF)-BETA-1 AND TGF-BETA-1-RECEPTOR REGULATION BY EPIDERMAL GROWTH-FACTOR IN A HUMAN ENDOMETRIAL CANCER CELL-LINE IK-90

作者：SAKATA M^*; KURACHI H; IKEGAMI H; JIKIHARA H; MORISHIGE K; MIYAKE A; TERAKAWA N; TANIZAWA O

来源：International Journal of Cancer, 1993, 54(5): 862-867.

DOI：10.1002/ijc.2910540523

Transforming growth factor-beta1 (TGF-beta1) enhanced cell proliferation in a concentration-dependent manner in a human endometrial cancer cell line, IK-90. Scatchard analysis of TGF-beta1 receptor in IK-90 cells, using I-125-TGF-beta1 as a ligand, revealed the presence of a class of high-affinity TGF-beta1 receptors (2,000 sites per cell, K(D) = 74pM). Moreover, IK-90 cells produced and secreted TGF-beta1: TGF-beta1 messenger RNA was detected at 2.5 and 4.0 kb by Northern-blot analysis using P-32-labeled TGF-beta1 cDNA as a probe, and TGF-beta1 activity in conditioned medium by the inhibition of H-3-thymidine uptake into CCI 64 mink lung epithelial cells. We investigated the regulation of TGF-beta1 receptor by 4 kinds of growth factor: epidermal growth factor (EGF) but not TGF-beta1, insulin or insulin-like growth factor-I increased the level of TGF-beta1 binding sites in a concentration- and time-dependent manner. These findings suggest that TGF-beta1 may be a potential autocrine growth factor in a human endometrial cancer cell line IK-90 and that this autocrine mechanism may be affected by EGF.

• 出版日期1993-7-9