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Involvement of the c‐ erb B‐2 oncogene product in the egf‐induced cell motility of sk‐ov‐3 ovarian cancer cells
Author(s) -
Wiechen Kai,
Karaaslan Selma,
Dietel Manfred
Publication year - 1999
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19991029)83:3<409::aid-ijc18>3.0.co;2-#
Subject(s) - motility , cancer research , ovarian cancer , oncogene , cancer , medicine , biology , microbiology and biotechnology , cell cycle
The epidermal growth factor (EGF) induces the rapid formation of dendritic processes and the dissociation of SK‐OV‐3 ovarian cancer cells. The SK‐OV‐3 cell line is characterized by over‐expression of the c‐ erb B‐2 oncogene product (p185 c‐ erb B‐2 ). To investigate the role of p185 c‐ erb B‐2 in cell motility, a c‐ erb B‐2‐specific single‐chain antibody was expressed in SK‐OV‐3 cells using a retroviral expression vector. Eight individual clones expressing the single chain antibody were isolated. These clones have prominent retention of the cell‐surface p185 c‐ erb B‐2 . The EGF‐induced morphologic changes and cell motility of the single‐chain‐antibody‐expressing clones were strongly inhibited, as observed in cell dissociation and in transmigration experiments. However, the suppression of p185 c‐ erb B‐2 does not inhibit the motility signal elicited by 12‐ O ‐tetradecanoyl‐phorbol‐13‐acetate. These data indicate that the c‐ erb B‐2 oncogene product is essential to mediate the motility signal of EGF to SK‐OV‐3 ovarian cancer cells. The enhancement of tumor‐cell motility may be partially responsible for the unfavorable prognosis of ovarian cancer with over‐expression of c‐ erb B‐2. Int. J. Cancer 83:409–414, 1999. © 1999 Wiley‐Liss, Inc.