Abstract
Endometrial cancer develops as a result of abnormal cell growth associated with uncontrolled cell proliferation, excessive activation of signaling pathways and miRNA activity. The aim of this study was to determine the expression profile of genes associated with cell proliferation and to assess which miRNAs can participate in the regulation of their expression. The study enrolled 40 patients with endometrial cancer and 10 patients without neoplastic changes. The expression profile of genes associated with cell proliferation and the expression profile of miRNAs were assessed using microarrays. RT-qPCR was performed to validate mRNA microarray results. The mirTAR tool was used to identify miRNAs that regulate the activity of genes associated with cell proliferation. Decreased expression of IGF1 and MYLK, as well as SOD2 overexpression, were observed in endometrial cancer using both mRNA microarrays and RT-qPCR. Microarray analysis showed low levels of NES and PRKCA, but this was only partially validated using RT-qPCR. Reduced activity of MYLK may be caused by increased miR-200c, miR-155 and miR-200b expression. Cell proliferation is disturbed in endometrial cancer, which may be associated with an overexpression of miR-200a, miR-200c, and miR-155, making it a potential diagnostic marker.
Highlights
Endometrial cancer develops as a result of abnormal growth of the cells, which in consequence acquire the ability to migrate and invade surrounding tissues
Carcinogenesis is associated with the disruption of cell cycle regulation, which leads to uncontrolled cell proliferation. It is caused by excessive activation of signaling pathways involved in stimulating cell growth
The aim of this study was to determine the expression profile of genes associated with cell proliferation and to assess which miRNAs can participate in the regulation of their expression
Summary
Endometrial cancer develops as a result of abnormal growth of the cells, which in consequence acquire the ability to migrate and invade surrounding tissues. The highest incidence concerns women in the peri- and postmenopausal period [1]. It is possible to distinguish two types of endometrial cancer according to clinical–pathological and molecular characteristics. Type I (estrogen-dependent) accounts for 80% of endometrial cancer cases, and progesterone and estrogen receptors are expressed in cancer tissue. The formation of type II cancer is not dependent on estrogenic stimulation, and progesterone and estrogen receptors usually are not expressed [1,2,3]. Endometrial cancer can be divided according to the degree of histological differentiation: G1 (≤5% solid growth pattern), G2 (6–50% solid growth pattern), G3 (>50% solid growth pattern) [4]
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