LAUSR

As an endocrine and metabolic disorder, polycystic ovarian syndrome (PCOS) is common in females at childbearing age. Our work was intended to uncover the underlying role of LINC00173 and its potential regulatory mechanism in PCOS based on two cell lines (PCOS granulosa cells and KGN cells) and an in vivo model established from Sprague Dawley rats. It was revealed that LINC00173 and JAG1 expressions were upregulated, while miR-124-3p was poorly expressed in PCOS patients and PCOS rats. Functional assays showed that LINC00173 overexpression repressed proliferation and stimulated apoptosis in granulosa cells and KGN cells, while LINC00173 downregulation exhibited the opposite effects. Besides, it was verified that LINC00173 upregulated JAG1 expression in KGN cells via competitively binding to miR-124-3p. Similarly, miR-124-3p abundance was inversely related to LINC00173 and JAG1 level in PCOS. Subsequently, rescue assays elucidated that miR-124-3p upregulation or downregulation eliminated the effects on KGN cell proliferation and apoptosis mediated by LINC00173 overexpression or knockdown. In addition, it was found that the JAG1 level in KGN cells was adversely modulated by miR-124-3p and positively modulated by LINC00173. Moreover, it was further demonstrated that the reduced cell vitality and increased apoptosis of KGN cells induced by overexpressing LINC00173 could be relieved by JAG1 deletion. These findings suggested that LINC00173 could be a latent regulating factor for PCOS progression via modulating the miR-124-3p/JAG1 cascade.