Dysregulation of microRNAs (miRs) is implicated in the carcinogenesis of various types of malignant tumor by manipulating cell growth and apoptosis. Abnormal expression of miR‑320a is involved in tumorigenesis of many types of cancer. The potential association of miR‑320a and the possible regulatory mechanisms in endometrial carcinoma is rarely elucidated. In the present study, it was demonstrated that miR‑320a expression was decreased in endometrial carcinoma tissues and cell lines. The present results also indicated that overexpression of miR‑320a suppressed cell proliferation through inducing G2/M phrase arrest and apoptosis. Insulin‑like growth factor receptror‑1 (IGF‑1R) was verified to be the potential target of miR‑320a by computational analysis and luciferase reporter assays. In addition, overexpression of miR‑320a reduced endogenous IGF‑1R expression in cells. Furthermore, it was demonstrated that upregulation of miR‑320a inhibited phosphorylated (p)‑protein kinase B and p‑mechanistic target of rapamycin activation and promoted B cell lymphoma‑2‑associated death promoter expression. Reintroduction of IGF‑1R into miR‑320a‑overexpressed cells antagonized the impact of miR‑320a on its downstream protein, which demonstrated that the tumor suppressive role of miR‑320a in endometrial carcinoma is exerted by the signal pathway mediated by IGF‑1R. It was therefore concluded that miR‑320a served an anti‑tumor role on endometrial carcinoma through the regulation of IGF‑1R, and miR‑320a may be used as the target for the gene therapy of endometrial carcinoma.