Hambek Markus, Baghi Mehran, Strebhardt Klaus, May Angelika, Adunka Oliver, Gstöttner Wolfgang, Knecht Rainald
Department of Otorhinolaryngology, School of Medicine, J. W. Goethe University, 60590 Frankfurt, Germany.
Anticancer Res. 2004 Nov-Dec;24(6):3881-6.
Proliferation of squamous cell carcinoma of the head and neck (SCCHN) depends on epidermal growth factor receptor (EGFR) expression. As STAT 3 activation as well contributes to the cell growth in SCCHN, the interaction of STAT 3 and the EGFR is of great interest when considering treatment options through inhibition of STAT 3. We, therefore, evaluated the influence of blocking or activating the EGFR in human SCCHN cell lines and in vivo tumors on STAT 3 activation. We compared the effects on STAT 3 activation with the regulation of MAP Kinase under these conditions. We found that STAT 3 can be strongly inhibited via EGFR blocking in vitro as well as in vivo. However, the influence of EGFR regulation on the MAP Kinase pathway seemed to be very slight. These findings provide evidence that STAT 3 signal activity in head and neck carcinomas, which is partially responsible for proliferative activity, can be controlled via the EGFR.
头颈部鳞状细胞癌(SCCHN)的增殖依赖于表皮生长因子受体(EGFR)的表达。由于STAT 3的激活也对头颈部鳞状细胞癌的细胞生长有促进作用,因此在考虑通过抑制STAT 3来选择治疗方案时,STAT 3与EGFR之间的相互作用备受关注。因此,我们评估了阻断或激活人SCCHN细胞系及体内肿瘤中的EGFR对STAT 3激活的影响。我们比较了在这些条件下对STAT 3激活的影响与对MAP激酶调节的影响。我们发现,在体外和体内,通过阻断EGFR均可强烈抑制STAT 3。然而,EGFR调节对MAP激酶途径的影响似乎非常轻微。这些发现提供了证据,表明头颈部癌中部分负责增殖活性的STAT 3信号活性可通过EGFR来控制。