STAT 3 activation in head and neck squamous cell carcinomas is controlled by the EGFR.
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STAT 3 activation in head and neck squamous cell carcinomas is controlled by the EGFR. / Hambek, Markus; Baghi, Mehran; Strebhardt, Klaus; Strebhard, Klaus; May, Angelika; Adunka, Oliver; Gstöttner, Wolfgang; Knecht, Rainald.
In: ANTICANCER RES, Vol. 24, No. 6, 6, 2004, p. 3881-3886.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - STAT 3 activation in head and neck squamous cell carcinomas is controlled by the EGFR.
AU - Hambek, Markus
AU - Baghi, Mehran
AU - Strebhardt, Klaus
AU - Strebhard, Klaus
AU - May, Angelika
AU - Adunka, Oliver
AU - Gstöttner, Wolfgang
AU - Knecht, Rainald
PY - 2004
Y1 - 2004
N2 - 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.
AB - 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.
M3 - SCORING: Zeitschriftenaufsatz
VL - 24
SP - 3881
EP - 3886
JO - ANTICANCER RES
JF - ANTICANCER RES
SN - 0250-7005
IS - 6
M1 - 6
ER -