The cancer tissues of 21 patients with EC （tumor group） and 39 patients with non-EC （control group） and human endometrial cancer RL95-2 cells and 293T cells were selected as the subjects. The clinical data such as age， height， body mass （BM）， body mass index （BMI）， systolic blood pressure （SBP）， diastolic blood pressure （DBP）， waist circumference （WC） and abdominal circumference （AC） of the patients in tumor group and control group were collected. The levels of triglyceride（TG），total cholesterol （TC）， low-density lipoprotein （LDL）， high density lipoprotein （HDL）， Ki-67 and low-density lipoprotein receptor （LDLR） of the patients in two groups were measured.Bioinformatics method was used to predict the expression of target gene LDLR related to the proliferation and invasion downstream of miR-152. Real-time fluorescence quantitative PCR （RT-qPCR） method was used to detect the expression level of miR-152 in endometrial tissue of the patients in tumor group and control group， Western blotting method and immunohistochemistry were used to detect the expression levels of LDLR protein in endometrial tissue of the patients in tumor group and control group， and Person correlation analysis was used to analyze the correlations between the expression of LDLR mRNA and the general data， biochemical indexes of the patients and miR-152 expression. The RL95-2 cells were divided into empty plasmid group （transfected with miR-NC empty plasmid）， miR-152 group （transfected with miR-152-mimics）， miR-152-mimics+pcDNA3.1-vector group （simultaneously transfected with miR-152-mimics and pcDNA3.1-vector）， and miR-152-mimics+pcDNA3.1-LDLR group （simultaneously transfected with miR-152-mimics+pcDNA3.1-LDLR）. The proliferation rates of the EC cells in various groups were detected by CCK-8 method， and the number of invasive EC cells in various groups was detected by Transwell assay. The luciferase activities of the 293T cells in various groups were detected by double luciferase reporter gene experiment.

The expression level of miR-152 in endometrial tissue of the patients in tumor group was significantly lower than that in control group （P<0.05）， and the expression levels of LDLR mRNA and protein were higher than those in control group （P<0.05 or P<0.01）. The results of dual-luciferase reporter gene assay showed that LDLR was the target gene of miR-152.The Person correlation analysis results showed that the expression of LDLR mRNA in endometrial tissue of the patients in tumor group had a positive correlation with Ki-67， BMI， TC， TG， BM，and WC （r=0.4490， r=0.4377， r=0.4472， r=0.4706， r=0.5882， r=0.5130， P<0.05）， and it was negatively correlated with the expression of miR-152（r=－0.4378， P<0.05）. Compared with empty plasmid group， the proliferation rate of the RL95-2 cells in miR-152 group was decreased （P<0.05）， and the number of invasive cells was decreased （P<0.05）； compared with miR-152-mimics+pcDNA3.1-vector group， the proliferation rate of the cells in miR-152-mimics+pcDNA3.1-LDLR group was increased （P<0.01）， and the number of invasive cells was increased （P<0.01）.

MiR-152 inhibits the proliferation and invasion of the EC cells by decreasing the expression of LDLR.