Effects of Tra2-beta1 on proliferation, apoptosis, and metastasis of hypoxic endometrial carcinoma cell and its correlation with clinicopathological features.

Abstract

BackgroundThis study aims to examine the influence of human transformer-2-beta1 (Tra2-beta1) on endometrial carcinoma (EC) development. The effects of Tra2-beta1 on the proliferation, apoptosis, invasion, and cell cycle of EC cells were also investigated.MethodsFunctional in vitro experiments were performed on Tra2-beta1 knockdown cells and hypoxic model cells. Western blot was used to detect HIF-1a, vascular endothelial growth factor (VEGF), and Tra2-beta1 protein expression; CCK8 assay was used to detect cell proliferation; flow cytometry was used to detect apoptosis and cell cycle, and Transwell assay was used to detect cell invasion ability. Tumor specimens were collected from 128 consecutive patients to detect the expression of Tra2-beta1, and the relationship between and EC and Tra-beta1 were analyzed by clinical pathological data, which included lymph node metastasis, pathological types, histological grade, myometrial invasion, etc.ResultsTra2-beta1 was highly expressed in EC and was associated with clinical pathological features. It was related to the prognosis, and was found to promote proliferation (F=48.3, P<0.001) and migration (P<0.05), and inhibit apoptosis (P<0.05). Statistical analyses revealed a positive correlation between Tra2-beta1 and HIF-1a (correlation coefficient =0.36, P<0.001) and VEGF protein (correlation coefficient =0.23, P=0.021). In the hypoxic cell group and the combined intervention group, cell proliferation after 72 h was 9,783±45.6 and 6,783±68.4 (P<0.001), while the number of invasive cells was 421±16.8 and 276±11.2 (P<0.001), respectively. The apoptosis rates were 0.45±0.03 and 1.28±0.16, respectively (P<0.05).ConclusionsThe present findings demonstrate that the development of EC is positively correlated with Tra2-beta1. Tra2-beta1 may reverse the effect of hypoxia on EC, and this may provide new insights into the occurrence and development of EC.