scholarly journals UDP‐glucose dehydrogenase expression is upregulated following EMT and differentially affects intracellular glycerophosphocholine and acetylaspartate levels in breast mesenchymal cell lines.

2021 ◽  
Author(s):  
Qiong Wang ◽  
Sigurdur Trausti Karvelsson ◽  
Freyr Johannsson ◽  
Arnar Ingi Vilhjalmsson ◽  
Lars Hagen ◽  
...  
1998 ◽  
Vol 274 (5) ◽  
pp. G945-G954 ◽  
Author(s):  
Michelina Plateroti ◽  
Deborah C. Rubin ◽  
Isabelle Duluc ◽  
Renu Singh ◽  
Charlotte Foltzer-Jourdainne ◽  
...  

The intestine is characterized by morphofunctional differences along the proximodistal axis. The aim of this study was to derive mesenchymal cell lines representative of the gut axis. We isolated and cloned rat intestinal subepithelial myofibroblasts raised from 8-day proximal jejunum, distal ileum, and proximal colon lamina propria. Two clonal cell lines from each level of the gut were characterized. They 1) express the specific markers vimentin, smooth muscle α-actin, and smooth muscle myosin heavy chain, revealed by immunofluorescence microscopy and 2) distinctly support endodermal cell growth in a coculture model, depending on their regional origin, and 3) the clones raised from the various proximodistal regions maintain the same pattern of morphogenetic and growth and/or differentiation factor gene expression as in vivo: hepatocyte growth and/or scatter factor and transforming growth factor-β1 mRNAs analyzed by RT-PCR were more abundant, in the colon and ileal clones and mucosal connective tissue, respectively. In addition, epimorphin mRNA studied by Northern blot was also the highest in one ileal clone, in which it was selectively upregulated by all-trans retinoic acid (RA) treatment. Epimorphin expression in isolated 8-day intestinal lamina propria was higher in the distal small intestine and proximal colon than in the proximal small intestine. In conclusion, we isolated and characterized homogeneous cell subtypes that can now be used to approach the molecular regulation of the epithelium-mesenchyme-dependent regional specificity along the gut.


2007 ◽  
Vol 7 (Suppl 2) ◽  
pp. A59
Author(s):  
Sandra Sagmeister ◽  
Maria Eisenbauer ◽  
Christine Pirker ◽  
Klaus Holzmann ◽  
Wolfram Parzefall ◽  
...  

1983 ◽  
Vol 8 (2) ◽  
pp. 119-126
Author(s):  
Ryojin Uchino ◽  
Manabu Fukumoto ◽  
Toshihiro Adachi ◽  
Osamu Midorikawa

2007 ◽  
Vol 28 (2) ◽  
pp. 193-202 ◽  
Author(s):  
Karen L. Price ◽  
David A. Long ◽  
Nipurna Jina ◽  
Helen Liapis ◽  
Mike Hubank ◽  
...  

Many molecules have been implicated in kidney development, often based on experimental animal studies with organ cultures and cell lines. There are very few studies, however, that have directly addressed equivalent living human embryonic tissues. We generated renal mesenchymal cell lines from normal human metanephroi and used a microarray strategy to define changes in gene expression after stimulation with growth factors which enhance nephrogenesis in rodents. Changes were observed in 1) genes modulating diverse general cellular processes, such as matrix metalloproteinase 1 and stanniocalcin 1; 2) genes previously implicated in organogenesis e.g., sprouty 4 and midline 1; and 3) genes involved in blood vessel growth, including angiopoietin 1 and 4. Expression of these same genes was subsequently confirmed in vivo. Our novel data have identified several previously unhighlighted genes that may be implicated in differentiation programs within early human nephrogenesis.


2018 ◽  
Vol 26 ◽  
pp. S150 ◽  
Author(s):  
M. Piñeiro-Ramil ◽  
R. Castro-Viñuelas ◽  
C. Sanjuro-Rodríguez ◽  
T. Hermida-Gómez ◽  
I. Fuentes-Boquete ◽  
...  

2017 ◽  
Vol 37 (1) ◽  
Author(s):  
Shan Qin ◽  
Yanfang Li ◽  
Xuexia Cao ◽  
Jiexian Du ◽  
Xianghua Huang

A key transcription factor associated with poor prognosis and resistance to chemotherapy in ovarian cancer is NANOG. However, the mechanism by which NANOG functions remains undefined. It has been suggested that epithelial-to-mesenchymal transition (EMT) also contributes to development of drug resistance in different cancers. We thus determined whether NANOG expression was associated with EMT and chemoresistance in epithelial ovarian cancer cells. NANOG expression was increased in epithelial ovarian cancer cell lines compared with its expression in normal epithelial ovarian cell lines. NANOG expression in SKOV-3 or OV2008 cells directly correlated with high expression of mesenchymal cell markers and inversely with low expression of epithelial cell marker. RNAi-mediated silencing of NANOG in SKOV-3 reversed the expression of mesenchymal cell markers and restored expression of E-cadherin. Reversibly, stable overexpression of NANOG in Moody cells increased expression of N-cadherin whereas down-regulating expression of E-cadherin, cumulatively indicating that NANOG plays an important role in maintaining the mesenchymal cell markers. Modulating NANOG expression did not have any effect on proliferation or colony formation. Susceptibility to cisplatin increased in SKOV-3 cells on down-regulating NANOG and reversible results were obtained in Moody cells post-overexpression of NANOG. NANOG silencing in SKOV-3 and OV2008 robustly attenuated in vitro migration and invasion. NANOG expression exhibited a biphasic pattern in patients with ovarian cancer and expression was directly correlated to chemoresistance retrospectively. Cumulatively, our data demonstrate that NANOG expression modulates chemosensitivity and EMT resistance in ovarian cancer.


2017 ◽  
Author(s):  
Anh Viet-Phuong Le ◽  
Marcin Szaumkessel ◽  
Tuan Zea Tan ◽  
Jean-Paul Thiery ◽  
Erik W Thompson ◽  
...  

AbstractEpithelial-mesenchymal plasticity (EMP) is a dynamic process whereby epithelial carcinoma cells reversibly acquire morphological and invasive characteristics typical of mesenchymal cells, which facilitates metastasis. Understanding the methylation differences between epithelial and mesenchymal states may assist in the identification of optimal DNA methylation biomarkers for the blood-based monitoring of cancer. Methylation-sensitive high-resolution melting (MS-HRM) was used to examine the promoter methylation status of a panel of established and novel markers in a range of breast cancer cell lines spanning the epithelial-mesenchymal spectrum. Pyrosequencing was used to validate the MS-HRM results. The results indicate an overall distinction in methylation between epithelial and mesenchymal phenotypes. The mesenchymal expression markers VIM, DKK3 and CRABP1 were methylated in the majority of epithelial breast cancer cell lines while methylation of the epithelial expression markers GRHL2, MIR200C and CDH1 was restricted to mesenchymal cell lines. We also examined EMP association of several methylation markers that have been used to assess minimal residual disease. Markers such as AKR1B1 and APC methylation proved to be selective for epithelial breast cell lines, however RASSF1A, RARß, TWIST1 and SFRP2 methylation was seen in both epithelial and mesenchymal cell lines, supporting their suitability for a multi-marker panel.


2018 ◽  
Author(s):  
Yingping Liu ◽  
Hongfei Qiao ◽  
Jinglong Chen

AbstractBackgroundEMT has the crucial effect on the progression and metastasis of tumor. This work will elucidate the role of miR-425 in EMT and development of TNBC.MethodsThe differential miRNA expression among non-tumor, para-tumor (adjacent tissue of tumor) and tumor tissues was analyzed. The luciferase activities of TGF-β1 3’ UTR treated with miR-425 were determined. Then human breast cancer cell lines were dealt with mimics or inhibitors of miR-425, and then the cell proliferation and migration, invasion ability were assessed. The expression of TGF-β1 and markers of epithelial cell and mesenchymal cell were analyzed. The influences of miR-425 on development of TNBC through inducing EMT by targeting TGF-β 1 and TGF-β1/SMAD3 signaling pathway in TNBC cell lines were investigated. Furthermore, Xenograft mice were used to explore the potential roles of miR-425 on EMT and development of TNBC in vivo.ResultsCompared with non-tumor tissues, 9 miRNAs were upregulated and 3 miRNAs were down-regulated in tumor tissues. The relative expression of miR-425 in tumor tissues was obviously much lower than that in para-tumor and non-tumor tissues. MiR-425 suppressed TGF-β1 expression, additionally inhibited expression of mesenchymal cell markers, while exerted effects on cell proliferation and migration of TNBC cell lines. Moreover, the agomir of miR-425 could protect against development process in murine TNBC xenogarft model.ConclusionsOur results demonstrated that miR-425 targets to TGF-β1, and was a crucial suppressor on EMT and development of TNBC through inhibiting TGF-β1/SMAD3 signaling pathway. It suggested that aim at TGF-β1/SMAD3 signaling pathway by enhancing relative miR-425 expression, was a feasible therapy strategy for TNBC.


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