Chattopadhyay Naibedya, T-Felt Hansen Jacob, Godbole Madan M, Brown Edward M
Division of Endocrinology, Diabetes and Hypertension and Membrane Biology Program, Brigham and Women's Hospital, Harvard Medical School, 221 Longwood Avenue, Rm 205, Boston, MA 02115, USA.
Brain Res Mol Brain Res. 2004 Feb 5;121(1-2):146-50. doi: 10.1016/j.molbrainres.2003.11.008.
Transforming growth factor beta (TGFbeta) and hepatocyte growth factor (HGF) promote glioma progression. Using U87human astrocytoma cells, which express TGFbeta receptors (TbetaRs), we show (1) mRNA expression of Smads (2, 3, 4), bone morphogenetic protein (BMP)- and activin-A receptors; (2) TGFbeta1 inhibits and HGF induces proliferation; (3) TGFbeta1 and activin-A equipotently inhibit HGF secretion more than BMP-2, but none alters c-Met expression. Because interfering with TbetaR signaling might nullify the beneficial inhibition of HGF secretion, activin-A should instead be considered for combination glioma therapy.
转化生长因子β（TGFβ）和肝细胞生长因子（HGF）促进胶质瘤进展。利用表达TGFβ受体（TβRs）的U87人星形细胞瘤细胞，我们发现：（1）Smads（2、3、4）、骨形态发生蛋白（BMP）和激活素A受体的mRNA表达；（2）TGFβ1抑制而HGF诱导细胞增殖；（3）TGFβ1和激活素A抑制HGF分泌的能力相当，强于BMP-2，但均不改变c-Met表达。由于干扰TβR信号传导可能会消除对HGF分泌的有益抑制作用，因此在联合治疗胶质瘤时应考虑使用激活素A。
