Aim: Endometrial cell proliferation plays a critical role in adenomyosis. It has been reported that MIR22HG and miR-2861 play similar roles in regulating endometrial cell proliferation, indicating their involvement in adenomyosis. This study aimed to investigate the potential involvement of MIR22HG and miR-2861 in adenomyosis.
Methods: Endometrial biopsy was collected from both adenomyosis (n = 45) and the healthy controls (n = 45). The expression of MIR22HG and miR-2861 in biopsies were determined by quantitative reverse transcription polymerase chain reaction (RT-qPCR). The relationship between MIR22HG and miR-2861 in endometrial cells was analyzed by RT-qPCR. Methylation-specific PCR (MSP) was performed to analyze the effects of overexpression of MIR22HG on the expression of miR-2861. Western-blot assays were performed to illustrate the effect of MIR22HG, miR-2861, STAT3, and MMP2 on adenomyosis. Luciferase report assay was performed to analyze the interactions among miR-2861, STAT3, and MMP2. The role of MIR22HG and miR-2861 in regulating the proliferation of endometrial cells was analyzed by cell proliferation assay.
Results: The expression of MIR22HG and miR-2861 in adenomyosis did not change with menstrual cycle. MIR22HG and miR-2861 were significantly downregulated in adenomyosis and they were significantly and positively correlated with each other. In endometrial cells, overexpression of MIR22HG upregulated the expression of miR-2861 and decreased methylation of miR-2861 gene. MIR22HG and miR-2861 downregulated STAT3 and MMP2 to inhibit the proliferation of endometrial cells. In addition, overexpression of both MIR22HG and miR-2861 showed stronger effects.
Conclusion: MIR22HG is downregulated in adenomyosis and upregulates miR-2861 through demethylation to inhibit endometrial cell proliferation.
Keywords: MIR22HG; adenomyosis; methylation; miR-2861; proliferation.
© 2021 Japan Society of Obstetrics and Gynecology.