Study of IGFBP-3 in the Ovarian Carcinoma Cell Invasion
We have successfully established an ovarian cancer cell line (OVTW-59), which was derived
from an ovarian endometrioid carcinoma. Its sublines, labeled as P0, P1, P2, P3, and P4 with
increasing invasion abilities, were selected from transwell invasion chambers, where P0
represented the original cell line at 100th passage. By using cDNA microarray and verified
with quantitative reverse-transcriptase polymerase chain reaction, we have identified the
differentially gene expression profiles of these OVTW-59 series cell lines in order to
identify the invasion related suppressor and oncogenes from ovarian carcinoma. From these
genes, we selected insulin-like growth factor binding protein (IGFBP)-3, which is a
suppressor gene, and found it lower expressed in higher-grade tumors and correlated with
poor patient survival. In vitro, we found IGFBP-3 related to the inhibition of cancer cell
migration. In this study, we plan to setup stable transfected IGFBP-3 cell lines in P0 and
P4, and study the relationship among IGFBP-3, metalloproteinase-2 (our previous studies
which verified its relationship with tumor invasiveness) and insulin-like growth factor
(IGF)-1. We would study the changes in cytoskeletal structures and the known functions of
anti-proliferation and apoptosis in IGFBP-3. Furthermore, we would like to investigate the
mechanism of IGFBP-3 in the inhibition of invasion/migration of ovarian carcinoma, either
signaling through MAPK or PI3K/AKT pathways. Finally, through xenograft, we plan to study
for the possible application of IGFBP-3 in ovarian cancer therapy.
Interventional
Allocation: Non-Randomized, Endpoint Classification: Bio-availability Study, Intervention Model: Single Group Assignment, Masking: Single Blind, Primary Purpose: Diagnostic
migration, invasion, metastasis
Torng Pao-Ling, MD, PhD
Principal Investigator
Department of Obsteteric and Gynecology, National Tiawan University Hospital
Taiwan: Department of Health
9361700500
NCT00154986
August 2004
July 2005
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