| Summary: | 碩士 === 國防醫學院 === 微生物及免疫學研究所 === 99 === Among the gynecological tumors, the most lethal cancer is the ovarian cancer and about ninety percent of the ovarian cancers are from the epithelial tissue. In contrast to most other type of carcinomas, dissemination of ovarian cancers through vasculature is rare and exfoliation is the most common pathway for metastasis. Exfoliated tumor cells of ovarian cancers are transported by peritoneal fluid and implant on the peritoneum and mesothelial linings of pelvic and abdominal organs. The fluctuating expression of different molecules may play an important role in the processes of ovarian tumor development. These molecules not only help tumor cells to resist anoikis,but can lead to cell survival and proliferation due to activating AKT phosphorylation. Owing to evidences indicating that CD164 might play a role in metastasis of prostate cancer and CD164 can modulate the CXCL12-mediated migration by forming complex with CXCR4 in hematopoietic progenitor cells, we propose that the CD164, a sialomucin, may be involved in tumorigenesis and cancer metastasis. From the preliminary results we found that the expression of CD164 in ovarian epithelial cancer cell lines was higher than normal ovarian epithelial cells and depended on their malignancy. In OSE10, a normal epithelial ovarian cell line, overexpressing CD164 not only changed the cell morphology, but showed more colonies in anchorage-independent colony formation assay than wild-type and vehicle control cells, and the similar results were noted in human ovarian epithelial borderline cell lines, ML46 and in BEAS-2B, a lung normal epithelial cell line using the same assay. Then in the animal model we also found that CD164 overexpressing ovarian epithelial cells not only formed tumors, but grew faster than ovarian cancer cells. Furthermore, overexpression of CD164 caused up-regulation of E-cadherin and p-Akt but suppressed by CXCR4 inhibitor and PI3K inhibitor and the cell cycle was indeed affected. These results strongly suggest that CD164 is involved in the regulation of molecular mechanisms of ovarian tumor formation.
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