The differential expression of mRNAs and long noncoding RNAs between ectopic and eutopic endometria provides new insights into adenomyosis

Abstract

Adenomyosis, defined as ectopic endometrial tissue within the myometrium, can often be misdiagnosed as multiple uterine leiomyomata or endometrial thickening. We therefore performed a combined mRNA and long noncoding (lnc)RNA microarray and bioinformatic analysis of eutopic and ectopic endometria in women with adenomyosis to better understand its pathogenesis and help in the development of a semi-invasive diagnostic test. A total of 586 mRNAs were increased and 305 mRNAs decreased in the ectopic endometrium of adenomyosis compared with the eutopic endometrium, while 388 lncRNA transcripts were up-regulated and 188 down-regulated in ectopic compared with paired eutopic endometrial tissue. Bioinformatic analysis suggested a series of metabolic and molecular abnormalities in adenomyosis, which have many similarities with endometriosis. Furthermore, our study constitutes the first known report of lncRNA expression patterns in human adenomyosis ectopic and eutopic endometrial tissue.

Bioinformatics strategy for the screening of key genes to differentiate adenomyosis from endometriosis (Review)

“…Several researchers have performed a large-scale survey for the identification of differentially expressed genes (DEGs) between the eutopic and ectopic endometrium of women with endometriosis (6)(7)(8)(9)(10)(11). Some studies have examined the global transcriptome of isolated ectopic and eutopic tissues from women with adenomyosis (12)(13)(14). However, to date, to the best of our knowledge, there is no clear evidence to indicate that fundamental differences exist in the underlying mechanisms of disease development between adenomyosis and endometriosis.…”

“…The following data can be accessed via key word search: 'Adenomyosis AND ectopic AND human' [n=4, GEO accession nos. GSE68870 (14), GSE74373 (12), GSE78851 (13) and GSE7307]; and 'endometriosis AND ectopic AND human' [n=12, GEO accession nos. GSE68870 (14), GSE7307, GSE25628 (6), GSE40186 (7), GSE47359 (11), GSE51981 (8), GSE73948 (9), GSE94414, GSE99949, GSE105764 (10), GSE105765 (10) and GSE124010] (Table I).…”

“…In addition, to explore the proposed mechanisms of the pathogenesis of adenomyosis, the differential gene expression profiles were compared between ectopic and eutopic endometrial tissues of adenomyosis. Compared with the eutopic endometrium of women with adenomyosis, the major pathways in terms of highly significant functional networks in ectopic lesions of adenomyosis included ER signaling (steroid hormone responsiveness); cell death and survival signaling (proliferation, angiogenesis and apoptosis); cell-to-cell signaling (cell adhesion, interaction, movement and invasion); signaling involved in extracellular matrix remodeling; EMT signaling; would healing, scarring and fibrosis; oxidative damage signaling (oxidative phosphorylation); inflammatory and immune response; mitochondrial dysfunction; prostaglandin biosynthesis; and altered lncRNA and miRNA expression profiles (12)(13)(14)36,37,41,67,70,84,125,131,(135)(136)(137). Herndon et al reported that comparative transcriptomic analysis identified 1,024 DEGs, 140 upregulated and 884 downregulated genes, in the endometrium of women with and without adenomyosis (13).…”

Upregulation of long noncoding RNA TUG1 by EGR1 promotes adenomyotic epithelial cell migration and invasion through recruiting EZH2 and suppressing TIMP2

“…Our previous study suggested that lncRNA LINC00261 inhibits cell growth and migration in endometriosis (Sha et al, ). Zhou et al () and Jiang, Sun, Xue, Deng, and Wang, () identified many differentially expressed lncRNAs in the eutopic endometria of tissues with adenomyosis on a genome‐wide scale. However, to our knowledge, there are no studies that confirm the functional role of lncRNAs in adenomyosis.…”

Dysmenorrhea, Adenomyosis, Endometriosis, Tumor Process: Causation

“…Биоинформационный анализ метаболических и молекулярных нарушений, в частности аномальной экспрессии мРНК, показал множество общих черт, присущих аденомиозу и эндометриозу [7].…”