Role of TRPM i̇on channels in the process that goes from simple endometrial hyperplasia to endometrium cancer

Endometrium cancer is the most common type of gynecological cancer in the world. Every year, 287. 100 women are diagnosed with this condition. Endometrium cancer is the 4th most common cancer among women and 8th in deaths caused by cancer. Endometrial hyperplasia is the only known direct cause of endometrium cancer. Transformation of malignant cells due to increased proliferation, impaired differentiation, losing the ability to suicide are the main ways of abnormal tissue growth. As a result, uncontrolled expansion and invasion may occur. The transformation may routinely happen via changes in ion channel expression. Ion channels located in the plasma membrane are in charge of cellular electrogenesis and current flow. These channels are responsible for doing all basic behaviors of cells, like; apoptosis, proliferation, and differentiation. Ion channels' contribution to these essential tasks involves several main mechanisms. These are; protecting membrane potential, modulating cell volume and influx of basic signal transporting ions. The result is an abnormal progression of cellular response. Despite, the proposition of differential expression and ion channel activities that modulate cancer's appearance and progression; examining ion channel-dependent mechanisms in bladder cancer would be valuable. In our study, we included 20 patients each, diagnosed with: atypical endometrial hyperplasia, nonatypical endometrial hyperplasia, grade 1 endometrium adenocarcinoma, grade 2 endometrium adenocarcinoma, grade 3 endometrium adenocarcinoma in the last 10 years in our clinics by selecting fractional curettage (FRC) materials from the pathology archive. Expressions of those tissues are studied immunohistochemically and mRNA expressions of TRPM2 and TRPM7 were studied by a real-time polymerase chain reaction. We studied the effects of TRPM ion channels on endometrial carcinoma formation and our results not only shines light on whether TRPM2 and TRPM7 could be therapautic targets but we also think that these ion channels could be the new target genes in endometrial carcinoma and as a result, may enable further studies to target those proteins in vivo conditions in an effort to try experimental treatment modalities for endometrial carcinoma. In conclusion, TRPM7 miRNA and TRPM2 miRNA had lowered significantly in the transformation of endometrial hyperplasia to endometrial adenocarcinoma. While TRPM7 also lowered immunohistochemically in endometrial adenocarcinoma; TRPM2 didn't show any significant immunohistochemical change. TRPM7 and TRPM2 ion channels behave differently in different cancer types. Key words: Endometrium hyperplasia, endometrium adenocancer, TRPM2,TRPM7