RESUMEN
Osteoporosis and resulting fractures affect a significant group of people in the world. It has been shown in many studies that selenium has positive effects on bone metabolism. Based on this information, the aim of this study is to investigate whether bone differentiation will start in a shorter time by applying selenomethionine (SeMet) to hFOB cells.First, hFOB 1.19 cells were cultured. Safe doses of SeMet were determined by MTT and LDH tests. Ossification levels were determined by alizarin red staining and measurement of alkaline phosphatase enzyme levels. The results were analyzed with statistical tests.It was observed that SeMet increased cell viability at concentrations of 10, 25, 50, 100, and 200 µM in 24 h. At these concentrations, cell viability increased above the control, the viabilities were as follows: 109.4%, 104.9%, 104.3%, 103.15%, and 100.27%. High doses of SeMet significantly reduce cell viability. According to Alizarin red staining, SeMet increases the amount of calcium deposits in hFOB cells in a dose-dependent manner. In the experimental groups, the highest ALP enzyme was determined in the 7-day SeMet application. The most effective dose was measured as 15 µM.It was determined that SeMet, which is found as a trace element in living things in nature, increases the viability of hFOB cells, which are osteoblast cell precursors, and increases osteoblastic differentiation and osteoblastic activity in these cells. Our results are at a level that sheds light on an important problem in public health.
RESUMEN
Colorectal cancer poses a significant global health challenge, with a considerable proportion arising from colon adenomas. Understanding the molecules involved in the carcinogenesis process is crucial for improving colon cancer diagnosis and prognosis. While research on the role of epiplakin in cancer remains limited compared to other plakin group proteins, comprehending its expression patterns and correlations can offer valuable insights into colon carcinogenesis. In this study, we analyzed 60 tissue samples, including colon adenocarcinomas, tubular adenomas (low malignancy risk group), tubulovillous adenomas (high malignancy risk group), and adjacent normal colon tissues. Classification and grading were reevaluated by histological examination. Immunohistochemistry was performed to assess epiplakin and Ki67 expression. Epiplakin optical density and the Ki67 proliferation index were calculated using ImageJ. Statistical analyses were conducted to evaluate correlations and significance. Epiplakin expression was significantly decreased in colon adenocarcinomas [optical density median 4.04 (95% CI, 3.98 to 4.24)] and tubulovillous adenomas [4.32 (95% CI, 4.08 to 4.32)] compared to normal colon tissues [4.61 (95% CI, 4.50 to 4.67)] and tubular adenomas [4.87 (95% CI, 4.67 to 4.88)] (P < 0.05). Moreover, adenoma groups exhibited higher proliferation indices (P < 0.05), and a positive correlation was found between epiplakin expression and the Ki67 proliferation index (r = 0.317, P < 0.05). Our study highlights the potential significance of epiplakin in colorectal cancer. Decreased epiplakin expression is associated with colon malignancy progression, suggesting its role as a potential marker.