scholarly journals The Lnc RNA SPRY4-IT1 Modulates Trophoblast Cell Invasion and Migration by Affecting the Epithelial-Mesenchymal Transition

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Qing Zuo ◽  
Shiyun Huang ◽  
Yanfen Zou ◽  
Yetao Xu ◽  
Ziyan Jiang ◽  
...  
Keyword(s):  
Cell Invasion ◽  
Epithelial Mesenchymal Transition ◽  
Trophoblast Cell ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration

Interleukin-27 Inhibits Trophoblast Cell Invasion and Migration by Affecting the Epithelial–Mesenchymal Transition in Preeclampsia

2018 ◽  
Vol 26 (7) ◽  
pp. 928-938 ◽  
Author(s):  
Huisheng Ge ◽  
Nanlin Yin ◽  
Ting-Li Han ◽  
Dongni Huang ◽  
Xuehai Chen ◽  
...  
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Trophoblast Cell ◽  
Trophoblast Invasion ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Signal Transducer ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
Epithelial Phenotype ◽  
And Migration

Preeclampsia (PE) is a pregnancy-specific disorder representing a major cause of maternal and perinatal morbidity and mortality. Invasive and migratory phenotypes are acquired by trophoblasts through the process of epithelial–mesenchymal transition (EMT). Studies have shown that trophoblast EMT events are dysregulated in PE and play an important role in its development. Dysregulation of interleukin (IL)-27 and IL-27R (T-cell cytokine receptor (TCCR)/WSX -1) is relevant to PE. In this study, our results demonstrated that IL-27 did not significantly affect the proliferation and apoptosis of HTR -8/SVneo trophoblast cells, while it did significantly inhibit trophoblast invasion and migration. The expression of EMT-related proteins in HTR-8/SVneo cells and extravillous explants was detected after treatment with IL-27. Expression of epithelial markers was increased, and mesenchymal marker expression was reduced. Furthermore, we found that IL-27 could induce significant phosphorylation of Signal Transducer and Activator of Transcription 1 (STAT1) and Signal Transducer and Activator of Transcription 3 (STAT3) in a time-dependent manner in HTR-8/SVneo cells. Selective inhibitors of STAT1 (STAT1 siRNA) and STAT3 (STAT3 siRNA) were used to determine whether both STAT1 and STAT3 are required for IL-27-mediated inhibition of EMT. STAT1 inhibition in IL-27-treated cells attenuated the IL-27 effect, while the inhibition of STAT3 activation had no effect on the development of the epithelial phenotype. These results demonstrate that IL-27 may inhibit trophoblast cell migration and invasion by affecting the EMT process through an STAT1-dominant pathway in PE.

scholarly journals Galectin-1 From Cancer-Associated Fibroblasts Promotes the Invasion and Metastasis of Gastric Cancer Through TGF-β1-Induced Epithelial-Mesenchymal Transition

2021 ◽  
Author(s):  
xiaolan you ◽  
Jian Wu ◽  
Xiaojun Zhao ◽  
Xingyu Jiang ◽  
Wenxuan Tao ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Invasion ◽  
Epithelial Mesenchymal Transition ◽  
Cancer Associated Fibroblasts ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration ◽  
Tgf Β1

Abstract Background The gastric cancer (GC) microenvironment has important effects on biological behaviors, such as tumor cell invasion and metastasis. However, the mechanism by which the GC microenvironment promotes GC cell invasion and metastasis is unknown. The present study aimed to clarify the effects and mechanism of galectin-1 (GAL-1, encoded by LGALS1) on GC invasion and metastasis in the GC microenvironment.Methods The expression of GAL-1/ LGALS1 was determined using western blotting, immunohistochemistry, and quantitative real-time reverse transcription PCR in GC tissues. Besides, methods including stable transfection, Matrigel invasion and migration assays, and wound-healing assays in vitro; and metastasis assays in vivo, were also conducted.Results GAL-1 from cancer-associated fibroblasts (CAFs) induced the epithelial‑mesenchymal transition (EMT) of GC cells though the transforming growth factor beta (TGF-β1)/ Sma- and mad-related protein (Smad) pathway, and affected the prognosis of patients with GC. The level of GAL-1 was high in CAFs, and treating MGC-803 and SGC -7901 cell line with the conditioned medium from CAFs promoted their invasion and metastasis abilities. Overexpression of LGALS1 promoted the expression of TGF-β1 and induced EMT of GC cell lines. A TGF-β1 antagonist inhibited the invasion and migration of GC cells. In vivo, overexpression of LGALS1 promoted GC growth and metastasis, and the TGF-β1 antagonist dramatically reversed these events. Conclusions These findings suggested that high expression of GAL-1 in the GC microenvironment predicts a poor prognosis in patients with GC by promoting the migration and invasion of GC cells via EMT through the TGF-β1/Smad signaling pathway. The results might provide new therapeutic targets to treat GC.

scholarly journals Periostin Mediates TGF-β-Induced Epithelial Mesenchymal Transition in Prostate Cancer Cells

2015 ◽  
Vol 36 (2) ◽  
pp. 799-809 ◽  
Author(s):  
Qingfeng Hu ◽  
Shijun Tong ◽  
Xiaojun Zhao ◽  
Weihong Ding ◽  
Yuancheng Gou ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Western Blot ◽  
Cancer Cells ◽  
Cell Invasion ◽  
Associated Factors ◽  
Epithelial Mesenchymal Transition ◽  
Prostate Cancer Cells ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration

Background: In our previous study, we found that periostin was upregulated in prostate cancer, and its expression could be modulated by TGF-β. TGF-β could upregulate periostin expression in some cells, and both TGF-β and periostin could induce epithelial mesenchymal transition (EMT). We aimed to study the effect of periostin in the process of TGF-β-induced EMT in prostate cancer cells. Methods: We constructed a lentivirus vector containing the periostin gene and transduced it into PC3 and DU145 cells. After confirming periostin overexpression by PCR and Western blotting, we used an MTT assay to establish a growth curve to measure cell proliferation. Additionally, we performed transwell and wound healing assays to measure cell invasion and migration, respectively. Lastly, we measured the expression of EMT associated factors using Western blot analysis to test the effect of periostin on EMT in prostate cancer cells. Results: PCR and Western blot analyses confirmed that periostin was upregulated after infection with the periostin lentiviral vector. Periostin overexpression promoted increased cell proliferation, invasion, and migration as measured by MTT, transwell, and wound healing assays, respectively. Western blot analysis illustrated that periostin overexpression increased the expression of EMT associated factors, and periostin overexpression activated Akt and GSK-3β, which could be inhibited using a PI3K inhibitor. Additionally, TGF-β increased the levels of STAT3, Twist1 and periostin, while both STAT3 shRNA and Twist1 shRNA inhibited periostin expression. However, STAT3 shRNA also decreased Twist1 expression. Although reduction of STAT3, Twist1 or periostin levels with shRNA inhibited TGF-β-induced overexpression of EMT associated factors, periostin overexpression could reverse such inhibition by interfering with STAT3 and Twist1. Similarly, periostin overexpression also reversed inhibition of cell invasion induced by interference of STAT3 and Twist1. Conclusion: Our findings indicate that periostin is an important mediator of TGF-β-induced EMT and suggest that periostin is a potential therapeutic target for suppressing the metastatic progression of prostate cancer.

scholarly journals MicroRNA-484 promotes cell migration and invasion in non-small cell lung cancer

2020 ◽  
Author(s):  
Xiaoning Yang ◽  
Junfeng Ma ◽  
Fanghua Gong ◽  
Yu Liu
Keyword(s):  
Lung Cancer ◽  
Tumor Cell ◽  
Cell Invasion ◽  
Epithelial Mesenchymal Transition ◽  
Small Cell ◽  
Tumor Cell Invasion ◽  
Small Cell Lung ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration

Abstract Background Lung cancer is one of the most common causes of cancer-related deaths in the world, and non-small cell lung cancer (NSCLC) accounts for 85% of it. Studies have reported that microRNA-484 (miR-484) plays an important regulatory role in carcinogenesis and cancer development. Methods 25 clinical NSCLC samples were collected for microRNA array. The funvtion of miR-484 was investigated through Transwell and Mitgration assays. The expression levers of epithelial-mesenchymal transition (EMT) related factors were assessed by Western blot. Results miR-484 was up-regulated in tissues from NSCLC patients relative to tumor-adjacent normal tissues. Knocking-down miR-484 expression in A549 cells significantly suppressed tumor cell invasion and migration, suppressed epithelial-mesenchymal transition (EMT) process by increasing the expression of E-cadherin, and decreasing the expression of N-cadherin, vimentin, and MMP2. Upregulation of miR-484 expression in BEAS-2B normal lung epithelial cells significantly promoted tumor cell invasion and migration, decreased E-cadherin expression levels, and increased N-cadherin, vimentin, and MMP2 expression levels Conclusion miR-484 can promote tumor cell invasion and migration in NSCLC and may be a new target for NSCLC treatment.

scholarly journals High STRN Expression Promotes HCC Invasion and Migration but Not Cell Proliferation or Apoptosis through Facilitating Epithelial-Mesenchymal Transition

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Qian-yu Du ◽  
Jing-hao Yao ◽  
Yong-chun Zhou ◽  
Ling-jie Xu ◽  
Fu-you Zhao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Invasion ◽  
Tumour Cell ◽  
Epithelial Mesenchymal Transition ◽  
Morphological Changes ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
Huh7 Cells ◽  
And Migration ◽  
E Cadherin

A STRN-ALK fusion protein has been recently identified as a potential therapeutic target in multiple cancers; however, the role of STRN alone in regulating the biological function of hepatocellular carcinoma (HCC) remains unclear. In this study, we firstly detected an overexpression of STRN in HCC tissues compared to that in adjacent nontumour (ANT) tissues through IHC analysis, and the expression level of this protein was positively correlated with lymph node metastasis and TNM stage. In vitro, high expression of STRN was also confirmed in different HCC cell lines, and regulation of STRN expression in Huh7 cells did not significantly affect tumour cell proliferation or apoptosis but was positively correlated with tumour cell invasion and migration capacities. Moreover, both the knockdown and overexpression of STRN in Huh7 cells can lead to cell morphological changes that are accompanied with an alteration of epithelial-mesenchymal transition (EMT) molecular markers E-cadherin and Vimentin. Finally, STRN was further proved to be negatively related to E-cadherin expression but positively related to Vimentin expression in human HCC tissue samples. Taken together, STRN is upregulated in HCC and acts as a tumour promoter regulating cell invasion and migration through facilitating the EMT process.

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