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The etiology of polycystic ovary syndrome (PCOS) is complex and the pathogenesis is not fully understood. Some studies have shown that dysregulation of ovarian granulosa cells may be related to abnormal follicles and excessive androgen in women with PCOS. Our team has also confirmed the high expression status of  H19  in PCOS patients in the early stage. However, the relationship between  H19  and miR- 19b  in the development of PCOS is still unknown. Therefore, we used bioinformatics to predict the binding sites of human  H19  and miR- 19b , and of miR- 19b  and  CTGF  genes. After the silencing and overexpression of  H19 , real-time polymerase chain reaction (PCR) was used to detect the expressions of  H19 , miR- 19b , and  CTGF . Western blotting was used to detect CTGF protein. Proliferation of KGN cells after  H19  silencing was detected by CCK8. Flow cytometry was used to detect the apoptosis of KGN cells after  H19  silencing. After the overexpression of  H19 , it was found that the expression of miR- 19b  gene decreased and the expression of  CTGF  increased, whereas silencing of  H19  did the opposite. In addition,  H19  could promote cell proliferation and decrease cell apoptosis. Finally, luciferase reporter assays showed that the 3′-end sequences of lncRNA  H19  and  CTGF  contained the binding site of miR- 19b . In conclusion, our study indicated that lncRNA  H19  acted as a ceRNA to bind to miR- 19b  via a “sponge” to regulate the effect of  CTGF  on KGN cells, which may play a vital role in PCOS.

lncRNA H19 acts as a ceRNA to regulate the expression of CTGF by targeting miR-19b in polycystic ovary syndrome