The Effects of TGF-Beta on the Tumor Proliferation and Bone Resorption by Human Squamous Cell Carcinoma (S. C. C.)

研究了转化生长因子- β (tgf - β)对3种人口腔鳞状细胞癌细胞HSC-2、hsc - 3和HSC-4的影响。虽然这些细胞系对表皮生长因子同样敏感，但对tgf - β的反应是可变的。通过添加tgf - β观察到细胞生长和HSC-4 (^3H)-胸苷结合的剂量依赖性抑制作用，而对HSC-2和HSC-3的生长抑制作用是边际的。并观察了HSC-2、3、4对裸鼠颅骨骨吸收的影响。HSC-2和HSC-3能引起裸鼠颅骨骨吸收，而HSC-4不能。对tgf - β结合的Scatchard分析表明，所有鳞状细胞癌细胞系具有相似的结合特性，其中两类结合位点为tgf - β。^<125> i - tgf - β与细胞表面受体的亲和标记显示两个主要亲和交联带，m_r为65 kDa （type pei）和280 kDa （type III）。在所有被检查的鳞状细胞癌细胞系中都观察到85 kDa带的缺失（II型）。这些细胞系的I型受体数量是可变的：即HSC-4的I型受体相对于hsc -2,3的I型受体更为丰富。这些结果表明，sc细胞系的骨吸收与tgf - β对细胞生长的影响有关，这种影响可能是由I型受体介导的。

The effects of transforming growth Factor-beta (TGF-beta) on three human oral squamous cell carcinoma cell lines, HSC-2, 3, and HSC-4, were investigated. Although these cell lines were equally sensitive to epidermal growth factor, responses to TGF-beta were variable. Dose-dependent inhibition of cell growth and (^3H)-thymidine incorporation of HSC-4 was observed by addition of TGF-beta, whereas growth inhibitory effects on HSC-2 and HSC-3 were marginal. Also the bone resorptions at nude mice calvaria by HSC-2, 3, and HSC-4, were investigated. HSC-2 and HSC-3 were able to cause bone resorption of the nude mice calvaria, whereas HSC-4 was not. Scatchard analysis of the binding of TGF-beta suggested that all squamous cell carcinoma cell lines have similar binding properties, which two classes of binding sites for TGF-beta. Affinity labeling of ^<125>I-TGF-beta to cell surface receptors revealed the two major affinity cross-linked bands with M_rs of 65 kDa (typeI) and 280 kDa (type III). A concomitant loss of 85 kDa band (type II) was observed in all squamous cell carcinoma cell lines examined. The numbers of type I receptors of these cell lines are variable : That is type I receptors of HSC-4 are comparably more abundant than those of HSC-2,3. These results indicate that bone resorption by S.C.C. cell lines is related to TGF-beta's effect on cell growth of the cell lines and that these effects may be mediated by type I receptors.