| Summary: | Endometrial adenocarcinoma is a cancer that develops from the endometrium, from cells thatform the glands in the endometrium. Animal models such as the BDII rat have thecharacteristic property that they are prone to cancers, characterized by rapid tumor growth,that resemble human cancers. Such rat models are therefore used to study gene expression andsignal pathways in cancer. Cancer cells have the ability to invade surrounding tissues throughlymphatic and/or vascular circulation to produce secondary tumors at new sites. TheRho/ROCK pathway orchestrates cell motility thereby contributing in significantly tometastasis. ROCK, through phosphorylation of myosin phosphatase target subunit 1(MYPT1), inhibits MYPT1 and induces actomyosin contraction which contributes to manycellular processes. In this study, we were interested in investigating the expression of MYPT1and ROCK1 genes in malignant and non-malignant endometrial cell lines in BDII rat model,in human endometrial cancer cells represented by the Ishikawa cells line, and in humanembryonic kidney 293 (HEK293) human non-malignant control cells. Although statisticalsignificance was not reached due to the small sample size, a difference in the gene expressionlevels in malignant and non-malignant cells was observed. The results from the present studyshowed a higher expression of MYPT1 and ROCK1 genes in cancer cells (rat and human)compared to non-cancer cells, and we can conclude that this implicates the significance of theMYPT1/ROCK pathway in endometrial cancer and its deregulation.
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