ERβ-activated LINC01018 promotes endometriosis development by regulating the CDC25C/CDK1/CyclinB1 pathway  

作　　者：Ruihui Lu Jingwen Zhu Xin Li Cheng Zeng Yan Huang Chao Peng Yingfang Zhou Qing Xue 

机构地区：[1]Department of Obstetrics and Gynecology,Peking University First Hospital,Beijing 100034,China

出　　处：《Journal of Genetics and Genomics》2024年第6期617-629,共13页遗传学报（英文版）

基　　金：the National Natural Science Foundation of China(82271676)for funding support.

摘　　要：Endometriosis refers to as an estrogen-dependent disease.Estrogen receptorβ(ERB),the main estrogen receptor subtype which is encoded by the estrogen receptor 2(ESR2)gene,can mediate the action of estrogen in endometriosis.Although selective estrogen receptor modulators can target the ERβ,they are not specific due to the wide distribution of ERβ.Recently,long noncoding RNAs have been implicated in endometriosis.Therefore,we aim to explore and validate the downstream regulatory mechanism of ERβ,and to investigate the potential role of long intergenic noncoding RNA 1018(LINC01018)as a nonhormonal treatment for endometriosis.Our study demonstrates that the expression levels of ESR2 and LINCo1018 are increased in ectopic endometrial tissues and reveals a significant positive correlation between the ESR2 and LINCo1018 expression.Mechanistically,ERβdirectly binds to an estrogen response element located in the LINCO1018 promoter region and activates LINC01018 transcription.Functionally,ERβcan regulate the CDC25C/CDK1/CyclinB1 pathway and promote ectopic endometrial stromal cell proliferation via LINC01018 in vitro.Consistent with these findings,the knockdown of LINC01018 inhibits endometriotic lesion proliferation in vivo.In summary,our study demonstrates that the ERβ/LINC01018/CDC25C/CDK1/CyclinB1 signaling axis regulates endometriosis progression.

关 键 词：Estrogen receptorβ Long intergenic noncoding RNA 1018 (LINC01018) ENDOMETRIOSIS Cell cycle Proliferation 

分 类 号：Q255[生物学—细胞生物学]