Histol Histopathol

Original Article Open Access

MiR-195-5p suppresses gastric adenocarcinoma cell progression via targeting OTX1

Sizhe Hu1, Huanting Zhou2, Xiaokang Zhao1, Feng Qian1 and Cancan Jin1

1Department of Gastrointestinal Surgery and 2Department of Operating Room, Affiliated Dongyang People’s Hospital of Wenzhou Medical University, Dongyang, Zhejiang, China


Corresponding Author: Sizhe Hu, Department of Gastrointestinal Surgery, Affiliated Dongyang People’s Hospital of Wenzhou Medical University, 60 Wuning West Road, Dongyang, Zhejiang, 322100, China. e-mail: husizhe@zju.edu.cn


Summary. Gastric adenocarcinoma (GAC) caused by malignant transformation of gastric adenocytes is a malignancy with high incidence. MiR-195-5p modulates a variety of cancers. One of its target genes, orthodenticle homeobox 1 (OTX1), is believed to be a key modulator of tumor progression. We aim to analyze the mechanism of miR-195-5p and OTX1 in GAC. MiR-195-5p and OTX1 mRNA levels in GAC cells were tested via qRT-PCR. OTX1 protein and EMT-related protein levels were examined through western blot. Several cell functional assays were designed to measure changes in cell malignant behaviors. Dual luciferase assay verified the targeting relation of miR-195-5p and OTX1. These experimental results showed significantly low miR-195-5p expression and significantly high OTX1 expression in GAC cells. Enforced miR-195-5p level repressed cell malignant progression and accelerated cell apoptosis in GAC. Increased OTX1 weakened the above-mentioned effect caused by overexpressing miR-195-5p. Thus, miR-195-5p restrained migration, proliferation, invasion and epithelial-mesenchymal transition process of GAC cells, and promoted cell apoptosis through regulating OTX1. A new insight is provided for searching for biomarkers or therapeutic targets of GAC. Histol Histopathol 38, 659-668 (2023)

Key words: miR-195-5p, Gastric adenocarcinoma, OTX1, Invasion, Migration, Proliferation, Epithelial-mesenchymal transition

DOI: 10.14670/HH-18-512


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©The Author(s) 2023. Open Access. This article is licensed under a Creative Commons CC-BY International License.