miR-452-3p Targets Adenomatous Polyposis Coli to Regulate the Malignant Phenotypes and Prognosis of Esophageal Cancer.

Abstract

Background/aims: Esophageal cancer is a common malignancy of the digestive tract worldwide, with extremely poor prognosis in advanced stages. miR-452-3p regulates multiple tumors and may contribute to the development and progression of esophageal cancer. The current study aims to examine the correlation between miR-452-3p expression and prognosis in esophageal cancer and further investigate the potential molecular mechanisms by which miR-452-3p regulates the malignant phenotype of esophageal cancer cells.

Materials and methods: A total of 155 pairs of esophageal cancer tissues and adjacent normal tissue samples were collected. Reverse Transcription Quantitative PCR was used to detect the expression levels of miR-452-3p and adenomatous polyposis coli (APC). Survival analyses were performed using Kaplan-Meier and Cox regression analyses. The effects of miR-452-3p on the biological behavior of esophageal cancer cells were assessed through in vitro experiments. Additionally, dual-luciferase reporter gene assays and rescue experiments were performed to confirm the regulatory relationship between miR-452-3p and APC.

Results: The miR-452-3p expression is upregulated in esophageal cancer. Elevated miR-452-3p expression is closely related to the clinical pathological characteristics and poor prognosis of esophageal cancer and serves as an independent prognostic risk factor. Functional experiments demonstrate that miR-452-3p overexpression enhances the malignant biological behavior of esophageal cancer cells. miR-452-3p directly targets APC. Silencing APC reverses the inhibitory effect of miR-452-3p inhibitor on the malignant phenotype.

Conclusion: miR-452-3p promotes esophageal cancer progression by targeting APC, and patients with low levels of miR-452-3p exhibit favorable prognosis.