Xiaozhen Quan1, Meng Zhao1, Xuezhou Yang1, Yan Zhu2, Xiaolong Tian3. 1. Department of Reproductive Center, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang 441021, China. 2. Department of Obstetrics and Gynecology, Xiangyang Central Hospital, Affiliated Hospital Of Hubei University of Arts and Science, Xiangyang 441021, China. Electronic address: zhuyan_xycentral@163.com. 3. Department of Reproductive Center, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang 441021, China. Electronic address: litan0922@163.com.
Abstract
BACKGROUND: Long noncoding RNA LINC00511 has been identified to be aberrant expression and may as a tumor oncogene in various carcinomas. However, the potential role of LINC00511 in the onset of Preeclampsia (PE) pathogenesis remains unexplored. METHODS: Placental tissues from patients with PE were collected to detect expression levels of LINC00511 by qRT-PCR. Human HTR-8/SVneo trophoblast cell line was cultured, CCK-8 assay, wound healing assay and transwell assay were performed to determine the regulation of trophoblast biological function by LINC00511. Bioinformatics analysis, chromatin immunoprecipitation (ChIP), luciferases reporter assay were performed to verify the regulatory mechanism of LINC00511. RESULTS: LINC00511 was aberrantly down-regulated in placental tissues of PE patients. Overexpression of LINC00511 promoted trophoblast cell proliferation, migration and invasion. The transcription factor AP2γ directly binds to the promoter region of LINC00511 to activate transcription. In addition, LINC00511 was enriched in cytoplasm and functioned as a molecular spong for miR-29b-3p, antagonizing its ability to repress Cyr61 protein translation. CONCLUSION: This study demonstrated that AP2γ mediated downregulation of LINC00511 suppresses trophoblast invasion by regulating miR-29b-3p/ Cyr61 axis.
BACKGROUND: Long noncoding RNA LINC00511 has been identified to be aberrant expression and may as a tumor oncogene in various carcinomas. However, the potential role of LINC00511 in the onset of Preeclampsia (PE) pathogenesis remains unexplored. METHODS: Placental tissues from patients with PE were collected to detect expression levels of LINC00511 by qRT-PCR. HumanHTR-8/SVneo trophoblast cell line was cultured, CCK-8 assay, wound healing assay and transwell assay were performed to determine the regulation of trophoblast biological function by LINC00511. Bioinformatics analysis, chromatin immunoprecipitation (ChIP), luciferases reporter assay were performed to verify the regulatory mechanism of LINC00511. RESULTS:LINC00511 was aberrantly down-regulated in placental tissues of PE patients. Overexpression of LINC00511 promoted trophoblast cell proliferation, migration and invasion. The transcription factor AP2γ directly binds to the promoter region of LINC00511 to activate transcription. In addition, LINC00511 was enriched in cytoplasm and functioned as a molecular spong for miR-29b-3p, antagonizing its ability to repress Cyr61 protein translation. CONCLUSION: This study demonstrated that AP2γ mediated downregulation of LINC00511 suppresses trophoblast invasion by regulating miR-29b-3p/ Cyr61 axis.