EphA2, a possible target of miR-200a, functions through the AKT2 pathway in human lung carcinoma.

In this study, we searched possible targets of miR-200a in these subsets by IHC analyses focusing on the expression of known target proteins of miR-200a: beta-catenin, EphA2, ZEB1, PTEN, and YAP-1, as well as E-cadherin, the expression of which is suppressed by ZEB1. Among those 6 proteins, when all 38 cases of surgically resected specimens were analyzed as a whole, IHC score of ZEB1 was inversely (ρ=-.417) and E-cadherin was positively (ρ=.345) correlated with miR-200a expression. However, only EphA2 was inversely correlated with the expression of miR-200a in adenocarcinoma (ρ=-.496) and in pStage I/II group (ρ=-.547), while no correlation was seen in non-adenocarcinoma, squamous cell carcinoma, or pStage III carcinoma. Furthermore, by comparison of 3 groups categorized according to the AKT gene increase, only EphA2 was down-regulated to a statistically significant level in the AKT2+ group in both adenocarcinoma (p=.0447) and pStage I/II carcinoma (p=.0458). These results suggest that in lung carcinomas, higher Akt activation caused by increased AKT2 gene copy number leads to the upregulation of miR-200a, which exerts its function as a suppressor of EphA2 in adenocarcinoma and the early stages of carcinomas. PMID: 32922621 [PubMed]
Source: International Journal of Clinical and Experimental Pathology - Category: Pathology Authors: Tags: Int J Clin Exp Pathol Source Type: research