Publication Name	World Journal of Clinical Cases
Manuscript ID	48448
Country	China

Category	Medicine, Research & Experimental
Manuscript Type	Basic Study
Article Title	Reduced microRNA-451 expression in eutopic endometrium contributes to the pathogenesis of endometriosis
Manuscript Source	Unsolicited Manuscript
All Author List	Shan Gao, Shuang Liu, Zi-Ming Gao, Peng Deng and Dan-Bo Wang
Funding Agency and Grant Number
Corresponding Author	Dan-Bo Wang, MD, Professor, Department of Gynecology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, No.44 Xiaoheyan Road, Shenyang 110001, Liaoning, China. wangdb_cmu@126.com
Key Words	Endometriosis; miR-451; Proliferation; Apoptosis; Pathogenesis;
Core Tip	Despite the high prevalence of endometriosis, its etiology is unclear. This study focuses on the expression of miR-451 in patients diagnosed with endometriosis. We report miR-451 as a novel biomarker of endometriosis when it is downregulated in eutopic endometrium. YWHAZ, OSR1, TTN, and CDKN2D were identified as potential target genes of miR-451 that may have important roles in disease pathogenesis. We believe that our study contributes significantly to the literature because it suggests a novel biomarker for endometriosis that may facilitate early diagnosis of the disease without the need for invasive methods, such as laparoscopic examination.
Citation	Gao S, Liu S, Gao ZM, Deng P, Wang DB. Reduced microRNA-451 expression in eutopic endometrium contributes to the pathogenesis of endometriosis. World J Clin Cases 2019; 7(16): 2155-2164

Received	2019-05-13 02:38
Peer-Review Started	2019-05-21 00:49
To Make the First Decision	2019-07-31 02:58
Return for Revision	2019-08-01 02:24
Revised	2019-08-06 02:44
Second Decision	2019-08-16 11:45
Accepted by Journal Editor-in-Chief
Accepted by Company Editor-in-Chief	2019-08-20 04:04
Articles in Press	2019-08-20 04:04
Publication Fee Transferred
Edit the Manuscript by Language Editor	2019-08-21 10:02
Typeset the Manuscript	2019-08-23 00:53

ISSN	2307-8960 (online)
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