The level of RCAS1 expression is inversely correlated with the number of vimentin-positive stromal cells in epithelial ovarian cancer.
Expression of RCAS1 is significantly associated with clinical prognosis in 15 different types of human cancer. We have previously reported that RCAS1 expression is correlated with a decreasing number of vimentin-positive stromal cells in cervical cancer. Moreover, RCAS1 expression is related to the expression of matrix metalloprotease 1 and laminin 5 and angiogenesis. We examined whether RCAS1 contributes to connective tissue remodeling in epithelial ovarian cancer. RCAS1 expression was studied retrospectively via immunohistochemistry. Samples were obtained from resected tumor tissues from 65 patients with epithelial ovarian cancer. Statistical analysis was done to correlate RCAS1 expression and clinicopathologic variables. The associations between RCAS1 expression and the number of vimentin-positive cells or microvessel density were evaluated. Western blot analysis was also performed to verify the perturbation of vimentin expression in fibroblast L cells, following stimulation by soluble RCAS1. RCAS1 expression was detected in 72.3% (47/65 total cases) and significantly correlated with age and histological subtype. Patients with advanced stage, positive lymph node metastasis, or positive peritoneal cytological results had significantly shorter overall survival rates; however, no significant relationship was detected between RCAS1 immunoreactivity and overall survival. In the connective tissue surrounding tumor cells, the number of cells expressing vimentin significantly decreased in relation to the RCAS1 expression level. The growth of L cells was suppressed after stimulation by soluble RCAS1, and the expression of vimentin was markedly diminished. RCAS1 may contribute to connective tissue remodeling by altering the number of vimentin-positive cells in epithelial ovarian cancer.
Sonoda
Kenzo
K
Department of Obstetrics and Gynecology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. kenzo@med.kyushu-u.ac.jp
Miyamoto
Shingo
S
Kobayashi
Hiroaki
H
Ogawa
Shinji
S
Okugawa
Kaoru
K
Taniguchi
Shuichi
S
Wake
Norio
N
D000328:Adult; D000368:Aged; D000951:Antigens, Neoplasm / Q000378:metabolism*; D014408:Biomarkers, Tumor / Q000378:metabolism*; D015153:Blotting, Western; D005260:Female; D005347:Fibroblasts / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007124:Immunoenzyme Techniques; D055806:Microvessels; D008875:Middle Aged; D009367:Neoplasm Staging; D009375:Neoplasms, Glandular and Epithelial / Q000378:metabolism* / Q000401:mortality / Q000473:pathology; D010051:Ovarian Neoplasms / Q000378:metabolism* / Q000401:mortality / Q000473:pathology; D011379:Prognosis; D017154:Stromal Cells / Q000378:metabolism* / Q000473:pathology; D015996:Survival Rate; D014746:Vimentin / Q000378:metabolism*
D000951:Antigens, Neoplasm; D014408:Biomarkers, Tumor; C120762:EBAG9 protein, human; D014746:Vimentin