Abstract

Endometrial cancer remains the most common malignancy of the female genital system in developed countries. Tumor suppressor genes are responsible for controlling the cells fate in the cell cycle and preventing cancerogenesis. Gene expression affects cancer progression and is modulated by microRNAs defined as both tumor suppressors and oncogenes. These molecules indirectly regulate multiple processes like cell proliferation, differentiation and apoptosis. The aim of this study was to analyze miRNAs expression that can regulate the activity of tumor suppressor genes related to the cell cycle in patients with endometrioid endometrial cancer. The study group consisted of 12 samples that met the inclusion criteria from a total of 48 obtained. The 12 samples were used to analyze microRNA expression. Complementary miRNAs were identified using TargetScan Database and statistical analysis. MicroRNAs were determined for the tumor suppressor genes: CYR61, WT1, TSPYL5, HNRNPA0, BCL2L1 and BAK1. All the miRNAs were complementary to the described target genes based on TargetScan Database. There were five miRNAs differentially expressed that can regulate tumor suppressor genes related to the cell cycle. The distinguished miRNAs: mir-340-3p, mir-1236-5p, mir-874-3p, mir-873-5p.2 and mir-548-5p were differentially expressed in endometrial cancer in comparison to the control. Among the distinguished miRNAs, the most promising is mir-874-3p, which may have an important role in endometrial adenocarcinoma proliferation.

Highlights

  • Endometrial cancer (EC) remains the most common gynecological malignancy in developed countries, with more than 6000 newly diagnosed cases in Poland per year and 288 000 worldwide [1, 2]

  • We examined the gene expression of tumor suppressor genes related to the cell cycle [11]

  • The step was to assess which statistically significant miRNAs were able to interact with all distinguished tumor suppressor genes regulating the cell cycle

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Summary

Introduction

Endometrial cancer (EC) remains the most common gynecological malignancy in developed countries, with more than 6000 newly diagnosed cases in Poland per year and 288 000 worldwide [1, 2]. Type I endometrioid endometrial cancer (EEC), including G1 and G2 adenocarcinoma, arises from atypical endometrial hyperplasia and are pathogenetically related to unopposed estrogen stimulation. This type of EC occurs in peri- and postmenopausal age, with abnormal uterine bleeding in 90% of the patients. Tumor suppressor genes (TSGs) play a critical role in controlling the cell cycle assuring proper proliferation and differentiation. These genes prevent the accumulation of mutations and protect the cell from acquiring cancer phenotype by inducing apoptosis [7]. Many internal and external factors, including TSGs and miRNAs can affect the cell cycle by inhibiting or initiating cell division [9]

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