miR-141-3p inhibited BPA-induced proliferation and migration of lung cancer cells through PTGER4.

UNLABELLED

The chemical substance bisphenol A (BPA) is widely used in household products, and its effect on human health has frequently been the focus of research. The aim of this study was to explore the potential molecular regulatory mechanism of BPA on the proliferation and migration of lung cancer cells. In this study, the H1299 and A549 lung cancer cell lines were selected as the study objects. The cells were treated with different concentrations of BPA (0, 0.1, 1, or 10 μM), and cell viability, proliferation, and migration were evaluated by CCK-8, EdU, clonogenic, and scratch test assays. Western blotting and RT‒qPCR were used to detect the expression of related proteins and genes. Our findings indicated that BPA markedly enhanced both the proliferation and migration capacities of lung cancer cells. In BPA-treated lung cancer cells, the level of miR-141-3p was decreased, PTGER4 expression was significantly increased, and PTGER4 knockdown reduced BPA-induced lung cancer cell proliferation and migration. In addition, miR-141-3p can target and negatively regulate the expression of PTGER4 and further inhibit PI3K/AKT signaling pathway activation and MMPs expression. Moreover, PTGER4 overexpression weakened the inhibitory effect of the miR-141-3p mimic on the proliferation and migration of lung cancer cells. In conclusion, miR-141-3p can inhibit the proliferation and migration of BPA-induced lung cancer cells by downregulating PTGER4, providing a new potential target for the treatment and prevention of lung cancer.

SUPPLEMENTARY INFORMATION

The online version contains supplementary material available at 10.1007/s10616-024-00692-5.