Abstract
Endometriosis can cause severe social burdens. Abnormal circular RNA levels have been found to lead to changes of related gene expression, thereby mediating the occurrence and development of a series of diseases, including endometriosis. The role of circRNA in endometriosis is still in its infancy. This study will explore the role of circRNA hsa_circ_0063526 with microRNA-141-5p in the development of endometriosis. The expression levels of genes were detected by RT-qPCR. Transwell, wound-healing, and EdU assays were performed on the End1 / E6E7 cell line from the endometriosis patient. PCR and immunohistochemistry were used to detect the expression of candidate regulatory genes in ectopic lesions in an endometriosis mice model. The expression level of hsa_circ_0063526 in ectopic tissue of endometriosis patients was significantly higher than control (P<0.05), The expression levels of hsa_circ_0063526 and miRNA-141-5P in ectopic tissue of endometriosis were negatively correlated (P<0.05). Knockdown of hsa_circ_0063526 inhibited the invasion, migration, and proliferation ability of End1 / E6E7 cell; the inhibition of microRNA-141-5p rescued this inhibition (P <0.05). In vivo experiments showed that miR-141-5p and si-hsa_circ_0063526 treatment reduced lesion size and regulated endometriosis genes. Our data suggest that hsa_circ_0063526 and miR-141-5p are possible biomarkers and therapeutic targets for endometriosis.
Highlights
Endometriosis is a common estrogen-dependent chronic disease affecting about 10% of childbearing-aged women [1]
Previous studies from our group used miRNA Solexa sequencing and RT-qPCR verification to test the serum samples of endometriosis patients in stage I and II [16,17,18,19]; the results showed that the expression level of miR141 was lower than control [20]
The double luciferase assay showed that the co-transfection of hsa_circ_0063526 wild-type and the miR-141-5p mimic significantly reduced luciferase activity compared with the control group
Summary
Endometriosis is a common estrogen-dependent chronic disease affecting about 10% of childbearing-aged women [1]. The disease causes infertility and further malignant transformation, and 20-50% of infertile patients had endometriosis [2]. The etiology and pathogenesis of endometriosis are not clear. The cells continue to grow there, creating endometriosis [5]. Endometriosis has benign histomorphology, its clinical behaviors show similar malignant tumors' invasion and resistance to apoptosis [5]. The pathogenesis of endometriosis has been increasingly attributed to a variety of genes and factors closely related to genetics [6]. Current treatment for endometriosis has many side effects, including stopping the menstrual cycle [7,8,9,10]. New diagnostic indicators and non-hormonal therapy for endometriosis are urgently needed
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