Emodin Inhibits Migration and Invasion of Human Endometrial Stromal Cells by Facilitating the Mesenchymal–Epithelial Transition Through Targeting ILK

2016 ◽  
Vol 23 (11) ◽  
pp. 1526-1535 ◽  
Author(s):  
Qiaomei Zheng ◽  
Ying Xu ◽  
Jingjing Lu ◽  
Jing Zhao ◽  
Xuan Wei ◽  
...  
Keyword(s):  
Stromal Cells ◽  
Migration And Invasion ◽  
Endometrial Stromal Cells ◽  
Mesenchymal Epithelial Transition

Inhibition of METTL3/m6A/miR126 promotes the migration and invasion of endometrial stromal cells in endometriosis

2021 ◽  
Author(s):  
Xiaoou Li ◽  
Wenqian Xiong ◽  
Xuefeng Long ◽  
Xin Dai ◽  
Yuan Peng ◽  
...  
Keyword(s):  
Stromal Cells ◽  
Therapeutic Target ◽  
Molecular Mechanisms ◽  
Cellular Migration ◽  
Migration And Invasion ◽  
Diagnostic Biomarker ◽  
Rna Modifications ◽  
Normal Endometrium ◽  
Endometrial Stromal Cells ◽  
Ectopic Endometrium

Abstract N6-methyladenosine (m6A), one of the most abundant RNA modifications, is involved in the progression of many diseases, but its role and related molecular mechanisms in endometriosis remain unknown. To address these issues, we detected m6A levels in normal, eutopic and ectopic endometrium and found the m6A levels decreased in eutopic and ectopic endometrium compared with normal endometrium. In addition, we proved that methyltransferase-like 3 (METTL3) downregulation accounted for m6A reduction in endometriosis. Furthermore, we observed that METTL3 knockdown facilitated the migration and invasion of human endometrial stromal cells (HESCs), while METTL3 overexpression exerted opposite effects, suggesting that METTL3 downregulation might contribute to endometriosis development by enhancing cellular migration and invasion. Mechanistically, METTL3-dependent m6A was involved in the DGCR8-mediated maturation of primary microRNA126 (miR126, pri-miR126). Moreover, miR126 inhibitor significantly enhanced the migration and invasion of METTL3-overexpressing HESCs, whereas miR126 mimics attenuated the migration and invasion of METTL3-silenced HESCs. Our study revealed the METTL3/m6A/miR126 pathway, whose inhibition might contribute to endometriosis development by enhancing cellular migration and invasion. It also showed that METTL3 might be a novel diagnostic biomarker and therapeutic target for endometriosis.

scholarly journals Hypoxia-inducible factor-1α promotes endometrial stromal cells migration and invasion by upregulating autophagy in endometriosis

Reproduction ◽  
2017 ◽  
Vol 153 (6) ◽  
pp. 809-820 ◽  
Author(s):  
Hengwei Liu ◽  
Zhibing Zhang ◽  
Wenqian Xiong ◽  
Ling Zhang ◽  
Yao Xiong ◽  
...  
Keyword(s):  
Stromal Cells ◽  
Hypoxia Inducible Factor ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Ovarian Endometriosis ◽  
Endometrial Stromal Cells ◽  
Hypoxia Inducible Factor 1Α ◽  
Gynecological Disease ◽  
Benign Gynecological Disease ◽  
Ectopic Endometrium

Endometriosis is a benign gynecological disease that shares some characteristics with malignancy like migration and invasion. It has been reported that both hypoxia-inducible factor-1α (HIF-1α) and autophagy were upregulated in ectopic endometrium of patients with ovarian endometriosis. However, the crosstalk between HIF-1α and autophagy in the pathogenesis of endometriosis remains to be clarified. Accordingly, we investigated whether autophagy was regulated by HIF-1α, as well as whether the effect of HIF-1α on cell migration and invasion is mediated through autophagy upregulation. Here, we found that ectopic endometrium from patients with endometriosis highly expressed HIF-1α and autophagy-related protein LC3. In cultured human endometrial stromal cells (HESCs), autophagy was induced by hypoxia in a time-dependent manner and autophagy activation was dependent on HIF-1α. In addition, migration and invasion ability of HESCs were enhanced by hypoxia treatment, whereas knockdown of HIF-1α attenuated this effect. Furthermore, inhibiting autophagy with specific inhibitors and Beclin1 siRNA attenuated hypoxia triggered migration and invasion of HESCs. Taken together, these results suggest that HIF-1α promotes HESCs invasion and metastasis by upregulating autophagy. Thus, autophagy may be involved in the pathogenesis of endometriosis and inhibition of autophagy might be a novel therapeutic approach to the treatment of endometriosis.

Endometrial stromal cell proteomic analysis reveals LIM and SH3 protein 1 (LASP1) plays important roles in the progression of adenomyosis

2021 ◽  
Vol 27 (3) ◽  
Author(s):  
Faying Liu ◽  
Zengming Li ◽  
Jiubai Guo ◽  
Shufen Fang ◽  
Jiangyan Zhou ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Stromal Cells ◽  
Protein Identification ◽  
Molecular Mechanisms ◽  
Migration And Invasion ◽  
Dna Hypermethylation ◽  
Two Dimensional Gel Electrophoresis ◽  
Endometrial Stromal Cells ◽  
Invasion And Migration ◽  
Molecular Events

Abstract Adenomyosis is one of the most common gynecological disorders that the molecular events underlying its pathogenesis remain not fully understood. Prior studies have shown that endometrial stromal cells (ESCs) played crucial roles in the pathogenesis of adenomyosis. In this study, we utilized two-dimensional gel electrophoresis combined with protein identification by mass spectrometry (2D/MS) proteomics analysis to compare the differential protein expression profile between the paired eutopic and ectopic ESCs (EuESCs and EcESCs) in adenomyosis, and a total of 32 significantly altered protein spots were identified. Among which, the expression of LIM and SH3 protein 1 (LASP1) was increased significantly in EcESCs compared to EuESCs. Immunohistochemical assay showed that LASP1 was overexpressed in the stromal cells of ectopic endometriums compared to eutopic endometriums; further functional analyses revealed that LASP1 overexpression could enhance cell proliferation, migration and invasion of EcESCs. Furthermore, we also showed that the dysregulated expression of LASP1 in EcESCs was associated with DNA hypermethylation in the promoter region of the LASP1 gene. However, the detailed molecular mechanisms of enhancing cell proliferation, invasion and migration caused by upregulated LASP1 in adenomyosis needs further study. For the first time, our data suggested that LASP1 plays important roles in the pathogenesis of adenomyosis, and could serve as a prognostic biomarker of adenomyosis.

scholarly journals Ping-Chong-Jiang-Ni Formula Induces Apoptosis and Inhibits Proliferation of Human Ectopic Endometrial Stromal Cells in Endometriosis via the Activation of JNK Signaling Pathway

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Rui-Ning Liang ◽  
Pei-Shuang Li ◽  
Yang Zou ◽  
Yu-Ling Liu ◽  
Zhen Jiang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Stromal Cells ◽  
Migration And Invasion ◽  
Sprague Dawley ◽  
Childbearing Age ◽  
Endometrial Stromal Cells ◽  
Jnk Signaling ◽  
Jnk Signaling Pathway ◽  
Suppress Cell Proliferation

Endometriosis is a common gynecological condition in childbearing age women and its therapy in modern medicine achieves usually temporary cure. Ping-Chong-Jiang-Ni formula (PCJNF), a Chinese herbal medicine (CHM), was shown to be clinically effective on endometriosis. Meanwhile, c-Jun N-terminal kinase (JNK) signaling pathway was involved in the therapeutic process of CHM on endometriosis. Here, we explored the effect of PCJNF on the ectopic endometrial stromal cells (EESCs) from endometriosis and test whether JNK signaling was involved. After being treated with PCJNF-containing serum obtained from Sprague Dawley rat, cell proliferation, migration, invasion, and apoptosis were evaluated in EESCs, and the total and phosphorylated JNK, ERK, and p38 proteins were detected. Our results showed that PCJNF could suppress cell proliferation, migration, and invasion and induce apoptosis in EESCs. The suppressed proliferation and increased apoptosis were dependent on JNK activation. Additionally, PCJNF caused cell cycle arrest at G2/M phase and this effect was mediated by JNK signaling, while the decreased cell migration and invasion treated by PCJNF were independent of JNK signaling. In summary, our results provided the first evidence that PCJNF could suppress cell proliferation, migration, and invasion, while increasing apoptosis in EESCs, and the suppressed proliferation and enhanced apoptosis were mediated by JNK signaling.

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