文献类型：期刊文献

英文题名：The m6A methyltransferase METTL3 promotes trophoblast cell invasion by regulating MYLK expression

作者：Zhao, Jian[1,2];Ding, Haigang[1,2];Ding, Jinlong[1,2];Shi, Xiaoliang[1,2];He, Yao[1,2];Zhu, Hongdan[1,2];Yuan, Hua[1,2];Zhang, Tao[1,2,3];Zhang, Juan[1,2]

机构：[1]Shaoxing Matern & Child Hlth Care Hosp, Shaoxing 312000, Zhejiang, Peoples R China;[2]Shaoxing Univ, Obstet & Gynecol Hosp, Shaoxing 312000, Zhejiang, Peoples R China;[3]Shaoxing Women & Childrens Hosp, Shaoxing 312000, Zhejiang, Peoples R China

年份：2022

卷号：129

起止页码：1

外文期刊名：PLACENTA

收录：SCI-EXPANDED(收录号：WOS:000864743300001)、、Scopus(收录号：2-s2.0-85138610313)、WOS

基金：Funding This research was supported by the Zhejiang Provincial Natural Science Foundation of China (LGD20H040001) .

语种：英文

外文关键词：Preeclampsia; METTL3; MYLK; Trophoblast; Invasion

外文摘要：Introduction: The progression of placental diseases such as preeclampsia is closely related to trophoblast dysfunction. Recent studies indicated the dysregulation of N6-methyladenosine (m6A) RNA modification in trophoblast disorders, while the function of METTL3, a methyltransferase of m6A, in trophoblasts remains to be studied.Methods: The expression of METTL3 was determined by real-time PCR and immunoblotting. METTL3 expression in trophoblast cell lines HTR-8/SVneo and JEG-3 was knocked down using shRNA. The invasion of trophoblast cells in Matrigel was determined using xCELLigence. The m6A-containing transcripts was determined by m6A-sequencing in HTR-8/SVneo cells. The myosin light chain kinase (MYLK) gene was transfected into HTR-8/SVneo cells.Results: The expression of METTL3 was downregulated in preeclamptic placentae compared to normal placentae. Knockdown of METTL3 repressed the invasion of extravillous trophoblast cells. Mechanistically, METTL3 pro-moted the stability of MYLK mRNA through m6A modification. Overexpression of MYLK rescued retarded cell invasion by METTL3 depletion.Discussion: Collectively, our results highlight an essential role of METTL3-MYLK axis in trophoblast invasion.