Progress in understanding the relationship between long noncoding RNA and endometriosis

Yan, Wenying; Hu, Hsiao Yun; Tang, Biao

doi:10.1016/j.eurox.2019.100067

Cited by 12 publications

(10 citation statements)

References 48 publications

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“…In addition to miRNAs, some transcripts longer than 200 nucleotides lacking protein coding potential and transcribed by the RNA polymerase II (RNA Pol II), which are known as long non-coding RNAs (lncRNAs), may affect estrogen signaling by regulating the epigenetic status of protein-coding genes [123]. Together with the research progress on lncRNAs, there is increasing evidence that lncRNAs are involved in the pathogenesis of endometriosis [124]. For example, the lncRNA, HOTAIR, is upregulated by estradiol binding to the estrogen receptors, ERα and ERβ.…”

Section: Estrogen Receptors (Ers) and Estrogen-mediated Control Of Epmentioning

confidence: 99%

Estrogen- and Progesterone (P4)-Mediated Epigenetic Modifications of Endometrial Stromal Cells (EnSCs) and/or Mesenchymal Stem/Stromal Cells (MSCs) in the Etiopathogenesis of Endometriosis

Szukiewicz

Stangret

Ruiz‐Ruiz

et al. 2021

Stem Cell Rev and Rep

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Endometriosis is a common chronic inflammatory condition in which endometrial tissue appears outside the uterine cavity. Because ectopic endometriosis cells express both estrogen and progesterone (P4) receptors, they grow and undergo cyclic proliferation and breakdown similar to the endometrium. This debilitating gynecological disease affects up to 15% of reproductive aged women. Despite many years of research, the etiopathogenesis of endometrial lesions remains unclear. Retrograde transport of the viable menstrual endometrial cells with retained ability for attachment within the pelvic cavity, proliferation, differentiation and subsequent invasion into the surrounding tissue constitutes the rationale for widely accepted implantation theory. Accordingly, the most abundant cells in the endometrium are endometrial stromal cells (EnSCs). These cells constitute a particular population with clonogenic activity that resembles properties of mesenchymal stem/stromal cells (MSCs). Thus, a significant role of stem cell-based dysfunction in formation of the initial endometrial lesions is suspected. There is increasing evidence that the role of epigenetic mechanisms and processes in endometriosis have been underestimated. The importance of excess estrogen exposure and P4 resistance in epigenetic homeostasis failure in the endometrial/endometriotic tissue are crucial. Epigenetic alterations regarding transcription factors of estrogen and P4 signaling pathways in MSCs are robust in endometriotic tissue. Thus, perspectives for the future may include MSCs and EnSCs as the targets of epigenetic therapies in the prevention and treatment of endometriosis. Here, we reviewed the current known changes in the epigenetic background of EnSCs and MSCs due to estrogen/P4 imbalances in the context of etiopathogenesis of endometriosis.

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Section: Estrogen Receptors (Ers) and Estrogen-mediated Control Of Epmentioning

confidence: 99%

Estrogen- and Progesterone (P4)-Mediated Epigenetic Modifications of Endometrial Stromal Cells (EnSCs) and/or Mesenchymal Stem/Stromal Cells (MSCs) in the Etiopathogenesis of Endometriosis

Szukiewicz

Stangret

Ruiz‐Ruiz

et al. 2021

Stem Cell Rev and Rep

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“…As of now, pathogenesis of EMs remains unclear, but current evidence supports that EMs is correlated with an anomaly in uterus development. EMs is often the cause of infertility in women and treatment of EMs requires significant clinical tests and surgical treatment, with the administration of drugs that suppress the ovarian functions 5–10 . These drugs may harm the reproductive system and quality of life in women and often have a high incidence rate of postoperative complications.…”

Section: Introductionmentioning

confidence: 99%

“…These drugs may harm the reproductive system and quality of life in women and often have a high incidence rate of postoperative complications. Thus, it is imperative to explore effective targets in the treatment of EMs 5–10 …”

Section: Introductionmentioning

confidence: 99%

“…EMs is often the cause of infertility in women and treatment of EMs requires significant clinical tests and surgical treatment, with the administration of drugs that suppress the ovarian functions. [5][6][7][8][9][10] These drugs may harm the reproductive system and quality of life in women and often have a high incidence rate of postoperative complications. Thus, it is imperative to explore effective targets in the treatment of EMs.…”

Section: Introductionmentioning

confidence: 99%

“…Thus, it is imperative to explore effective targets in the treatment of EMs. [5][6][7][8][9][10] HOXA10, a homeobox gene, plays a key role as a transcription factor in uterus development that regulates the expression of many genes. [11][12][13] During the development of mammals, HOXA10 is involved in regulating the genital differentiation of the Mullerian duct, and HOXA10 is specifically and highly expressed in the uterine epithelium, stroma, and muscles during the development of the reproductive system.…”

Section: Introductionmentioning

confidence: 99%

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Lnc‐RNA LINC01279 induces endometriosis via targeting of HOXA10

Liu

Cheng

Wei

et al. 2021

J of Obstet and Gynaecol

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Aim To explore the regulatory role and molecular mechanism of lncRNA‐LINC01279 in endometriosis (EMs). Methods Between September 2018 and July 2019, 20 EMs patients and 20 healthy subjects were recruited to detect the expression of lncRNA‐LINC01279 in EMs and in normal endometrium via qRT‐PCR. Autograft was used to establish EMs models on Spraque–Dawley (SD) rats, which was followed by taking volume measurements of EMs endometrium and observing pathological changes in the morphology of EMs via hematoxylin and eosin (H&E) staining. The qRT‐PCR technique was further carried out to determine mRNA expression of lncRNA‐LINC01279 and HOXA10 in the serum of EMs rats and LINC01279 shRNA‐transfected rats, while the protein expression of HOXA10 was determined using a Western blot. Results EMs patients presented with upregulation of lncRNA‐LINC01279 and downregulation of HOXA10 (p < 0.01 or 0.001). Online predictions further revealed that lncRNA‐LINC01279 regulated the expression of HOXA10 via miRNA‐135b. In EMs models, it was observed that there were a significantly enlarged endometrium and poor pathological morphology, significant upregulation of lncRNA‐LINC01279, and downregulation of miR‐135b and HOXA10 in serum (p < 0.05, 0.01 or 0.001). In the lncRNA‐LINC01279 shRNA group, EMs rats, following treatment, had a sharp decrease in the volume of EMs endometrium, and an improvement in pathological morphology, while lncRNA‐LINC01279 was downregulated, with upregulation of miR‐135b and HOXA10 (p < 0.05, 0.01 or 0.001). Conclusion LncRNA‐LINC01279, by the mechanism of targeting miR‐135b, has the potential to downregulate the expression of HOXA10, and therefore, can promote the development and progression of EMs.

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