Molecular mechanism of mesenchymal-epithelial transition in peritoneal metastasis of ovarian cancer

Ovarian cancer is the most lethal cancer in gynecological malignancies. High-grade serous ovarian tumors are the most problematic group since they are mostly metastatic at the time of diagnosis. In this study, in serous ovarian carcinoma, transgenomic mRNA expressions were evaluated in primary tumor cell, metastatic tumor tissues and tumor cells in the ascites, thus attempting to reveal genetic alterations in level of gene expression, from the epithelial phenotype to mesenchymal phenotype, followed by epithelial phenotype again. There was significant difference in gene expressions between primary tumor and metastatic tissue in 7 genes; among cells obtained from primary tumor tissue and ascites in 1041 genes and between metastatic tissue and cells obtained from ascites in 648 genes(p≤0,05). In this context, cancer cells return to original epithelial phenotype by successive EMT-MET transformations to form metastatic foci, suggesting that expression changes between primary tumor and metastatic implant are small. Significant increases were observed in VTRNA1-1, which is effective in inhibiting apoptosis; MCAM expression, which have poor prognostic effect in ovarian-cancer, among tumor cells obtained from primary tumor and metastatic tissue. Among the tumor cells obtained from the primary tumor and ascites, significant expression differences were found in SNORD gene family, in MALAT1, which have been shown to be effective in proliferation and metastasis of ovarian cancer and in MUC1-gene, that are effective in cellular transformation and tumorigenesis (p≤ 0,05). The introduction of genes that are effective in metastatic process and their associated molecular mechanisms and pathways, will provide biomarkers and therapeutic targets.