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Tumor Biology |
Department of Obstetrics and Gynecology, Okayama University Medical School, Okayama 700-8558, Japan
The insulin-like growth factor I receptor (IGF-IR) plays an essential
role in the establishment and maintenance of transformed phenotype, and
interference with the IGF-IR pathway by antisense or dominant-negative
mutants causes reversal of the transformed phenotype in many rodent and
human tumor cell lines. We stably transfected an IGF-IR antisense mRNA
expression plasmid into human papillomavirus (HPV)-negative C33a cell
line, HPV-16-positive SiHa cell line, and HPV-18-positive HeLa S3 cell
line to determine whether the IGF-IR could be a target for cervical
cancer cells, especially in the presence of HPV. Approximately 30–80%
down-regulation of IGF-IR expression was observed by Western blot in
antisense transfected clones. There was a little inhibition in
monolayer growth in all cell lines. In C33a cells, wild-type and sense
clones formed 92–146 colonies in soft agar after 3 weeks; antisense
clones formed <12 colonies. In SiHa cells, wild-type and sense clones
formed 
60 colonies after 5 weeks; antisense clones formed 0–3
colonies. In HeLa S3 cells, wild-type and sense clones formed 218–291
colonies in soft agar after 2 weeks; antisense clones formed 14–160
colonies. There was a good correlation between IGF-IR down-regulation
level and inhibition of transformation in soft agar. Tumorigenesis in
nude mice was strongly inhibited in HeLa S3 and SiHa clones transfected
with the antisense. These results indicate that down-regulation of
IGF-IR by antisense RNA can reverse the transformed phenotype of human
cervical cancer cells, even when harboring malignant type HPVs.
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