Effect of the hsa‑microRNA 200c‑3p/ZEB1 loop in epithelial‑mesenchymal transition of ovarian cancer cells
Year: 2026
Type: article
Study design: Observational Study
Abstract: Ovarian cancer (OC) is a disease often diagnosed at advanced stages with distant metastasis, which is characterized by the epithelial-mesenchymal transition (EMT) of cells.The aim of the present study was to analyze the target genes of Homo sapiens microRNA 200c-3p (hsa-miR-200c-3p) and their associated proteins, which have a role in the EMT process.The expression level of hsa-miR-200c-3p was analyzed in ovarian tissues obtained from healthy individuals (n=15) and patients with advanced epithelial OC (EOC; n=15).Zinc finger enhancer-box binding homeobox 1 (ZEB1) is one of the target genes of hsa-miR-200c-3p and was identified using in silico methods.The expression level of ZEB1 was analyzed in both groups.ZEB1, vimentin and E-cadherin proteins were analyzed using immunohistochemistry (IHC) in healthy and OC tissues.The expression of hsa-miR-200c-3p was significantly increased in patients with OC (P<0.01).ZEB1 expression decreased significantly in the EOC group (P<0.01).The correlation analysis indicated a strong negative correlation between hsa-miR-200c-3p and the ZEB1 gene (ρ=-0.75;P<0.01).IHC staining revealed that the higher staining intensity of ZEB1 and E-cadherin proteins were found in cancerous tissues compared with healthy ones (P<0.05).However, the intensity and extent of vimentin staining was decreased in cancerous tissues (P<0.05).The decreased expression of ZEB1 is regulated by hsa-miR-200c-3p.The downregulation of ZEB1 may cause insufficient binding to the mRNA of E-cadherin, leading to increased E-cadherin expression.The hsa-miR-200c-3p/ZEB1 loop regulates vimentin and E-cadherin expression in OC.The increased expression level of hsa-miR-200c-3p may also cause mesenchymal-to-epithelial transition in OC cells.
Source: Oncology Letters
Institution: Istanbul University
Language: English
Subfield: Cancer Research
Domain: Life Sciences
Open Access status: diamond
OpenAlex ID: W7128498962