scholarly journals Berberine inhibits the proliferation, invasion and migration of endometrial stromal cells by downregulating miR‑429

2021 ◽  
Vol 23 (6) ◽  
Author(s):  
Yongjuan Gu ◽  
Zhigang Zhou
Keyword(s):  
Stromal Cells ◽  
Endometrial Stromal Cells ◽  
Invasion And Migration ◽  
And Migration

scholarly journals Low Expression of STING Promoted Endometrial Stromal Cells Invasion and Migration Via STING/IRF3/IFNb1 Pathway in Endometriosis Eutopic Endometrium

2021 ◽  
Author(s):  
zhen xu ◽  
hen zhao ◽  
caixin yue ◽  
lixia zhang ◽  
muzi li ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Stromal Cells ◽  
Chronic Inflammatory Disease ◽  
Glandular Epithelium ◽  
Normal Endometrium ◽  
Endometrial Stromal Cells ◽  
Eutopic Endometrium ◽  
Invasion And Migration ◽  
And Migration ◽  
Low Expression

Abstract Background: Recent studies have confirmed that endometriosis is a chronic inflammatory disease. In our previous work, we found that STING (stimulator of interferon genes) was differentially expressed in eutopic endometrium and controlled endometrium by proteomics.Method: we used the 11 pairs of samples to verify STING expression by WB and IHC experiments. We detected cells proliferation by EdU assays, cells invasion and migration by Transwell assays. The effect of signaling pathway in HESC was detected by WB and Elisa expreriments.Results: STING was significantly lower expressed in eutopic endometrium of endometriosis, while IHC results showed that STING was expressed in both stroma and glandular epithelium of normal endometrium, but in endometriosis, STING was mainly expressed in the stroma of eutopic endometrium, and mainly in glandular epithelium of ectopic endometrium. Further study on the role of STING on endometrial stromal cells showed that low expression of STING could promote the HESC proliferation by EdU experiments, invasion and migration by Transwell experiments. The effect of STING/IRF3/IFNb1 signaling pathway in HESC with low expression of STING was also reduced, mainly showed the decreased expression of phosphorylated IRF3 and TBK1, and the decreased secretion of IFNb1. In order to further study the effect of IFNb1, secreted by STING/ IRF3/IFNb1 signaling pathway, on stromal cells, we added exogenous IFNb1 to the HESC with low expression of STING, and found that IFNb1 could reverse the invasion and migration function of stromal cells, but little effect on cell proliferation.Conclusions: We clarified that STING expressed mainly in stromal tissues and lower in endometriosis eutopic endometrium compared to normal endometrium. Low expressed STING promoted stromal cells invasion and migration via STING/IRF3/IFNb1 signaling pathway.

scholarly journals T-cadherin inhibits invasion and migration of endometrial stromal cells in endometriosis

2019 ◽  
Vol 35 (1) ◽  
pp. 145-156 ◽  
Author(s):  
Qinsheng Lu ◽  
Yanqing Huang ◽  
Jiabao Wu ◽  
Yutao Guan ◽  
Miaomiao Du ◽  
...  
Keyword(s):  
Western Blot ◽  
Cell Invasion ◽  
Stromal Cells ◽  
Medical Center ◽  
Guangdong Province ◽  
Endometrial Stromal Cells ◽  
Eutopic Endometrium ◽  
Invasion And Migration ◽  
And Migration

Abstract STUDY QUESTION What is the expression level of T-cadherin in endometriosis, and does T-cadherin play a role in regulating invasion and migration of endometrial stromal cells? SUMMARY ANSWER T-cadherin expression was reduced in ectopic endometriotic lesions compared to eutopic endometrium, and T-cadherin overexpression inhibited the invasion and migration of endometrial stromal cells. WHAT IS KNOWN ALREADY Endometriosis is a disease that involves active cell invasion and migration. T-cadherin can inhibit cell invasion, migration and proliferation in various cancer cells, but its role in endometriosis has not been investigated. STUDY DESIGN, SIZE, DURATION We explored the expression status of T-cadherin in 40 patients with and 24 without endometriosis. We also isolated endometrial stromal cells to study the invasion, migration and signaling pathway regulation of T-cadherin overexpression. PARTICIPANTS/MATERIALS, SETTING, METHODS Patients were recruited at the Guangzhou Women and Children’s Medical Center to study the expression levels of T-cadherin. The expression of T-cadherin was detected by immunohistochemistry staining and western blot. H-score was used to evaluate the staining intensity of T-cadherin. The correlation between T-cadherin expression levels (H-score) and endometriosis patients’ age, stage, lesion size and adhesion was analyzed. Endometrial stromal cells from patients with and without endometriosis were isolated, and cell invasion and migration were detected by transwell assays after T-cadherin overexpression. The expression of vimentin in T-cadherin-overexpressed cells was detected by western blot. After T-cadherin overexpression, the phosphorylation profile of signaling pathway proteins was detected with the Proteome Profiler Human Phospho-Kinase Array Kit. MAIN RESULTS AND THE ROLE OF CHANCE There was no difference in the expression of T-cadherin in the normal endometrium of control patients and the eutopic endometrium of endometriotic patients, but it was significantly decreased in the ectopic endometrium of endometriotic patients, compared with control endometrium and eutopic endometrium of endometriosis patients (P < 0.0001, for both). Western blot analysis also showed that the expression of T-cadherin was decreased in ectopic endometriotic lesions, but not the normal control endometrium or the endometriotic eutopic endometrium. The results of transwell assays indicated that T-cadherin overexpression inhibited the invasion and migration of endometrial stromal cells. In addition, T-cadherin overexpression promoted the phosphorylation of HSP27 (S78/S82) and JNK 1/2/3 (T183/Y185, T221/Y223) and decreased the expression of vimentin, MMP2 and MMP9 in eutopic endometriosis stromal cells. LARGE-SCALE DATA N/A. LIMITATIONS, REASONS FOR CAUTION The control group were patients with benign gynecological conditions (e.g. uterus myoma, endometrial or cervical polyp), which may have genetic or epigenetic variations associated with T-cadherin expression and signaling pathways. The case numbers of involved endometriosis and control patients were limited. This study only used endometrial stromal cells from patients with or without endometriosis. Ideally, ectopic endometrial stromal cells of the ovarian endometriotic lesions should also be utilized to explore the function of T-cadherin. WIDER IMPLICATIONS OF THE FINDINGS Further investigation of the role of T-cadherin in endometriosis may generate new potential therapeutic targets for this complex disorder. STUDY FUNDING AND COMPETING INTEREST(S) This study was supported by the Natural Science Foundation of Guangdong Province (2016A030313495), National Natural Science Foundation of China (81702567, 81671406, 31871412), the Science and Technology Programs of Guangdong (2017A050501021), Medical Science Technology Research Fund of Guangdong Province (A2018075), the Science and Technology Programs of Guangzhou City (201704030103), Internal Project of Family Planning Research Institute of Guangdong Province (S2018004), Post-doc initiation fund of Guangzhou (3302) and Post-doc science research initiation fund of Guangzhou Women and Children’s Medical Center (20160322). There are no conflicts of interest.

scholarly journals USP10 promotes proliferation and migration and inhibits apoptosis of endometrial stromal cells in endometriosis through activating the Raf-1/MEK/ERK pathway

2018 ◽  
Vol 315 (6) ◽  
pp. C863-C872 ◽  
Author(s):  
Qiong Chen ◽  
Yuanyuan Hang ◽  
Tingting Zhang ◽  
Li Tan ◽  
Shuangdi Li ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Signaling Pathway ◽  
Stromal Cells ◽  
Uterine Cavity ◽  
Mitogen Activated Protein Kinase ◽  
Erk Signaling ◽  
Erk Pathway ◽  
Endometrial Stromal Cells ◽  
And Migration ◽  
Proliferation And Migration

Endometriosis has been initially described as endometrial-like tissue outside of the uterine cavity. The mitogen-activated protein kinase/ERK kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling pathway playing an important role in the regulation of cell proliferation, apoptosis, and migration has been found to be activated in endometriosis. However, regulation of the MEK/ERK signaling pathway in endometriosis has not been fully understood. In this study, primary-cultured endometrial stromal cells were collected from patients with endometriosis and healthy controls, and the proliferation, apoptosis, and migration of ectopic endometrial stromal cells transfected with ubiquitin-specific protease 10 (USP10)-small-interfering RNA (siRNA) or pLVX-Puro-USP10 with or without MEK inhibitor PD-98059 or exogenous signaling stimulation such as epidermal growth factor (EGF) were measured by CCK-8, flow cytometry, and Transwell, respectively. The gene and protein expressions were measured by real-time PCR or Western blot. USP10 overexpression promoted ectopic endometrial stromal cell migration and proliferation, suppressed cell apoptosis, and activated MEK/ERK signaling that is a critical downstream target of the serine/threonine protein kinase Raf-1, which was significantly blocked by PD-98059. USP10 silencing demonstrated the inverse effects, and these effects induced by USP10 silencing were significantly blocked by EGF. USP10 overexpression promoted Raf-1 protein expression, but not mRNA expression, through deubiquitination. In conclusion, these results suggest that USP10 promotes proliferation and migration and inhibits apoptosis of endometrial stromal cells in endometriosis through activating the Raf-1/MEK/ERK pathway.

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 Expression of Talin-1 in endometriosis and its possible role in pathogenesis

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Xian Tang ◽  
Qing Li ◽  
Lijie Li ◽  
Jianfa Jiang
Keyword(s):  
Cell Invasion ◽  
Expression Level ◽  
Migration And Invasion ◽  
Endometrial Stromal Cells ◽  
Invasion And Migration ◽  
Proliferation And Apoptosis ◽  
Mrna And Protein Expression ◽  
Polymerase Chain ◽  
And Migration

Abstract Background Endometriosis is a disease that involves active cell invasion and migration. Talin-1 can promote cell invasion, migration and adhension in various cancer cells, but its role in endometriosis has not been investigated. This study was to investigate the expression level of Talin-1 in endometriosis and the role of Talin-1 in the proliferation, adhesion, migration, and invasion of human endometrial stromal cells (ESCs). Methods Ectopic and eutopic endometrial tissues were collected from women with endometriosis, and the control endometrial tissues were obtained from patients without endometriosis. The expression level of Talin-1 was detected in each sample using quantitative real-time polymerase chain reaction and immunohistochemistry. The expression of Talin-1 was inhibited using RNA interference in ESCs, and its proliferation, apoptosis, adhesion, migration, and invasion capacity were analyzed. Western blotting was performed to detect the expression of related molecules after the downregulation of Talin-1. Results The results showed that the mRNA and protein expression of Talin-1 were significantly increased in the ectopic endometrium and eutopic endometrial tissues compared with the controls. The knockdown of Talin-1 did not affect the proliferation and apoptosis of ESCs. The results indicated that the downexpression of Talin-1 inhibited the adhesion, invasion, and migration of ESCs. In addition, the expressions of N-cadherin, MMP-2, and integrin β3 were significantly lower after the deregulation of Talin-1, whereas the levels of E-cadherin were significantly increased. Conclusions The expression of Talin-1 was increased in the ectopic and eutopic endometrial tissues compared with the control endometrium. The downregulation of Talin-1 inhibited the adhesion, invasion, and migration of ESCs.

scholarly journals Osteopontin Regulates Endometrial Stromal Cell Migration in Endometriosis through the PI3K Pathway

2020 ◽  
Author(s):  
Xiaoxia Fu ◽  
Mengyun Yao ◽  
Chaoshuang Ye ◽  
Tao Fang ◽  
Ruijin Wu
Keyword(s):  
Cell Migration ◽  
Stromal Cells ◽  
Pi3k Pathway ◽  
Immunofluorescence Assay ◽  
Phosphatidylinositol 3 Kinase ◽  
Migration Ability ◽  
Endometrial Stromal Cells ◽  
Tissue Invasion ◽  
And Migration ◽  
Proliferation And Migration

Abstract Endometriosis is generally characterized as a tumor-like disease because of its potential for distant metastasis and local tissue invasion, while whether osteopontin (OPN) plays a role in the pathogenesis of endometriosis has not been thoroughly investigated. We investigated the expression of OPN, urokinase plasminogen activator (uPA), phosphatidylinositol 3 kinase (PI3K), and phospho-PI3 kinase (p-PI3K) in endometrial stromal cells (ESCs). The serum concentration of OPN was determined by enzyme-linked immunosorbent assays (ELISA). OPN was downregulated to explore the corresponding change of uPA, p-PI3K, F-actin, and α-tubulin. The expression of OPN, uPA, PI3K, and p-PI3K was evaluated by western blot and quantitative real-time PCR (RT-qPCR) and the expression of F-actin and α-tubulin was confirmed by immunofluorescence assay. The proliferation and migration abilities of ESCs were investigated by CCK8, transwell, and wound scratch assays. Endometrial OPN, p-PI3K, and uPA expressions and serum OPN levels were increased in patients with endometriosis compared with the control. The expressions of p-PI3K, uPA, and α-tubulin were decreased by siRNA-OPN interference in ectopic ESCs. Activation and inhibition of the PI3K pathway apparently upregulate and downregulate uPA expression. Knockdown of OPN and inhibition of the PI3K pathway remarkably inhibited cell migration in ectopic ESCs. Meanwhile, activation of the PI3K pathway promoted the migration ability of ectopic ESCs. OPN may regulate the expression of uPA through the PI3K signal pathway to affect the migration ability of ESCs, indicating that OPN, uPA, and the PI3K pathway may be potential targets for interrupting development of endometriosis.

scholarly journals The Origin of Stroma Influences the Biological Characteristics of Oral Squamous Cell Carcinoma

Cancers ◽  
2021 ◽  
Vol 13 (14) ◽  
pp. 3491
Author(s):  
Haruka Omori ◽  
Qiusheng Shan ◽  
Kiyofumi Takabatake ◽  
Keisuke Nakano ◽  
Hotaka Kawai ◽  
...  
Keyword(s):  
Stromal Cells ◽  
Tartrate Resistant Acid Phosphatase ◽  
Bioinformatics Analyses ◽  
Invasion And Migration ◽  
Migration Assays ◽  
Tumor Parenchyma ◽  
And Migration

Normal stromal cells surrounding the tumor parenchyma, such as the extracellular matrix (ECM), normal fibroblasts, mesenchymal stromal cells, and osteoblasts, play a significant role in the progression of cancers. However, the role of gingival and periodontal ligament tissue-derived stromal cells in OSCC progression is unclear. In this study, the effect of G-SCs and P-SCs on the differentiation, proliferation, invasion, and migration of OSCC cells in vitro was examined by Giemsa staining, Immunofluorescence (IF), (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) (MTS), invasion, and migration assays. Furthermore, the effect of G-SCs and P-SCs on the differentiation, proliferation, and bone invasion by OSCC cells in vivo was examined by hematoxylin-eosin (HE) staining, immunohistochemistry (IHC), and tartrate-resistant acid phosphatase (TRAP) staining, respectively. Finally, microarray data and bioinformatics analyses identified potential genes that caused the different effects of G-SCs and P-SCs on OSCC progression. The results showed that both G-SCs and P-SCs inhibited the differentiation and promoted the proliferation, invasion, and migration of OSCC in vitro and in vivo. In addition, genes, including CDK1, BUB1B, TOP2A, DLGAP5, BUB1, and CCNB2, are probably involved in causing the different effects of G-SCs and P-SCs on OSCC progression. Therefore, as a potential regulatory mechanism, both G-SCs and P-SCs can promote OSCC progression.

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