MicroRNA‑29‑3p regulates the β‑catenin pathway by targeting IGF1 to inhibit the proliferation of prolactinoma cells.

The present study aimed to analyze the effects and underlying mechanisms of microRNA (miR)‑29‑3p on the proliferation and secretory abilities of prolactinoma cells by targeting insulin‑like growth factor (IGF)‑1/β‑catenin. The relationship between miR‑29a‑3p and the survival of prolactinoma cells was analyzed with the Kaplan‑Meier method in reference to The Cancer Genome Atlas. The expression levels of miR‑29a‑3p and IGF‑1 in MMQ and GH3 cells were detected. A dual‑luciferase reporter gene assay was performed to verify the combination of miR‑29a‑3p and IGF‑1. Cells were transfected with a miR‑29a‑3p mimic and/or IGF‑1 pcDNA3.1 to analyze the effects on the proliferation, apoptosis and secretion of prolactin (PRL) and growth hormone (GH) of prolactinoma cells. The effects on β‑catenin in the cytoplasm and nucleus were investigated by western blot analysis. The results showed that miR‑29a‑3p expression was low in MMQ and GH3 cells. Overexpression miR‑29a‑3p inhibited IGF‑1 mRNA and protein expression. miR‑29a‑3p inhibited cell proliferation and PRL and GH expression, and promoted apoptosis by inhibiting IGF‑1. Increasing the expression of miR‑29a‑3p increased β‑catenin levels in the cytoplasm, whereas IGF‑1 promoted β‑catenin activation and entry into the nucleus, and reversed the inhibitory effects of miR‑29a‑3p on β‑catenin. To conclude, miR‑29a‑3p inhibited the proliferation and secretory abilities of prolactinoma cells by inhibiting nuclear translocation of β‑catenin via a molecular mechanism that is inseparable from IGF‑1.