Annals of agricultural and environmental medicine : AAEM · 2026
miR-483-5p promotes uterine leiomyoma progression by targeting TIMP2.
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Fang Yanhui, Pan Wenyu, Jiang Junqiao, Hu Jing, Xu Qiuxia, Huang Liyuan, Chen Yating
Аннотация
INTRODUCTION AND OBJECTIVE: Uterine leiomyoma (UL) is a prevalent tumour of the female reproductive system which is poorly understood in terms of pathogenesis, and treatment options are limited. MicroRNAs (miRNAs) have been identified as being associated with tumorigenesis. The aim of the study is to elucide the function of miR-483-5p in promoting UL progression by targeting TIMP metallopeptidase inhibitor 2 (TIMP2) and its underlying molecular mechanisms.
MATERIAL AND METHODS: The study included 340 patients with UL. The expression level of miR-483-5p was measured using quantitative real-time PCR (qPCR). Following knockdown of miR-483-5p in uterine leiomyoma cells (UtLMCs), cell proliferation, migration, and apoptosis were assessed using CCK-8, Transwell, and flow cytometry assays. Subsequently, bioinformatics analysis and luciferase reporter gene detection identified the target of miR-483-5p.
RESULTS: Compared to the adjacent myometrium, miR-483-5p was upregulated in UL tissues. Experiments revealed that miR-483-5p expression levels were increased in UtLMCs. It was determined that TIMP2 is the direct target of miR-483-5p. Furthermore, miR-483-5p significantly promoted the proliferation and migration of UtLMCs, and inhibited their apoptosis by targeting TIMP2.
CONCLUSIONS: Collectively, these findings reveal the molecular mechanism by which miR-483-5p negatively regulates TIMP2 to promote UL development, providing new insights for the targeted therapy of UL.
MATERIAL AND METHODS: The study included 340 patients with UL. The expression level of miR-483-5p was measured using quantitative real-time PCR (qPCR). Following knockdown of miR-483-5p in uterine leiomyoma cells (UtLMCs), cell proliferation, migration, and apoptosis were assessed using CCK-8, Transwell, and flow cytometry assays. Subsequently, bioinformatics analysis and luciferase reporter gene detection identified the target of miR-483-5p.
RESULTS: Compared to the adjacent myometrium, miR-483-5p was upregulated in UL tissues. Experiments revealed that miR-483-5p expression levels were increased in UtLMCs. It was determined that TIMP2 is the direct target of miR-483-5p. Furthermore, miR-483-5p significantly promoted the proliferation and migration of UtLMCs, and inhibited their apoptosis by targeting TIMP2.
CONCLUSIONS: Collectively, these findings reveal the molecular mechanism by which miR-483-5p negatively regulates TIMP2 to promote UL development, providing new insights for the targeted therapy of UL.