An In Vitro Model of Posterior Capsular Opacity: SPARC and TGF-β2 Minimize Epithelial-to-Mesenchymal Transition in Lens Epithelium

2007 ◽  
Vol 48 (10) ◽  
pp. 4679 ◽  
Author(s):  
Norihito Gotoh ◽  
Nikole R. Perdue ◽  
Hiroyuki Matsushima ◽  
E. Helene Sage ◽  
Qi Yan ◽  
...  
Keyword(s):  
In Vitro Model ◽  
Epithelial To Mesenchymal Transition ◽  
Lens Epithelium ◽  
Mesenchymal Transition ◽  
Posterior Capsular Opacity ◽  
Vitro Model

scholarly journals An In Vitro Model That Recapitulates the Epithelial to Mesenchymal Transition (EMT) in Human Breast Cancer

PLoS ONE ◽  
2011 ◽  
Vol 6 (2) ◽  
pp. e17083 ◽  
Author(s):  
Elad Katz ◽  
Sylvie Dubois-Marshall ◽  
Andrew H. Sims ◽  
Philippe Gautier ◽  
Helen Caldwell ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
In Vitro Model ◽  
Epithelial To Mesenchymal Transition ◽  
Human Breast ◽  
Mesenchymal Transition ◽  
Vitro Model

scholarly journals The Histone Variant MacroH2A1 Impacts Circadian Gene Expression and Cell Phenotype in an In Vitro Model of Hepatocellular Carcinoma

Biomedicines ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 1057
Author(s):  
Annalucia Carbone ◽  
Elisabetta De Santis ◽  
Olga Cela ◽  
Vincenzo Giambra ◽  
Luca Miele ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
In Vitro Model ◽  
Epithelial To Mesenchymal Transition ◽  
Expression Patterns ◽  
Cell Phenotype ◽  
Alcoholic Fatty Liver ◽  
Mesenchymal Transition ◽  
Circadian Genes ◽  
Vitro Model

Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death worldwide. A foremost risk factor for HCC is obesity/metabolic syndrome-related non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH), which is prompted by remarkable changes in transcription patterns of genes enriching metabolic, immune/inflammatory, and circadian pathways. Epigenetic mechanisms play a role in NAFLD-associated HCC, and macroH2A1, a variant of histone H2A, is involved in the pathogenesis modulating the expression of oncogenes and/or tumor suppressor genes and interacting with SIRT1, which crucially impacts the circadian clock circuitry. Hence, we aimed to appraise if and how macroH2A1 regulated the expression patterns of circadian genes in the setting of NAFLD-associated HCC. We took advantage of an in vitro model of liver cancer represented by HepG2 (human hepatocarcinoma) cells stably knocked down for macroH2A1 and conducted whole transcriptome profiling and deep phenotyping analysis. We found up-regulation of PER1 along with several deregulated circadian genes, enriching several important pathways and functions related to cancer onset and progression, such as epithelial-to-mesenchymal transition, cell cycle deregulation, and DNA damage. PER1 silencing partially mitigated the malignant phenotype induced by the loss of macroH2A1 in HCC cells. In conclusion, our findings suggest a modulatory role for the core circadian protein PER1 in liver carcinogenesis in the context of a lack of the macroH2A1 epigenetic and transcriptional landscape.

Short-term effect of FSH on gene expression in bovine granulosa cells in vitro

2018 ◽  
Vol 30 (8) ◽  
pp. 1154 ◽  
Author(s):  
Anne-Laure Nivet ◽  
Isabelle Dufort ◽  
Isabelle Gilbert ◽  
Marc-André Sirard
Keyword(s):  
Gene Expression ◽  
Cellular Response ◽  
Epithelial To Mesenchymal Transition ◽  
Short Term ◽  
Mesenchymal Transition ◽  
Vitro Model ◽  
Cell Transcriptome ◽  
Physical Changes

In reproduction, FSH is one of the most important hormones, especially in females, because it controls the number of follicles and the rate of follicular growth. Although several studies have examined the follicular response at the transcriptome level, it is difficult to obtain a clear and complete picture of the genes responding to an increase in FSH in an in vivo context because follicles undergo rapid morphological and physical changes during their growth. To help define the transcriptome downstream response to FSH, an in vitro model was used in the present study to observe the short-term (4 h) cellular response. Gene expression analysis highlighted a set of novel transcripts that had not been reported previously as being part of the FSH response. Moreover, the results of the present study indicate that the epithelial to mesenchymal transition pathway is inhibited by short-term FSH stimuli, maintaining follicles in a growth phase and preventing differentiation. Modulating gene expression in vitro has physiological limitations, but it can help assess the potential downstream response and begin the mapping of the granulosa cell transcriptome in relation to FSH. This information is a key feature to help discriminate between the effects of FSH and LH, or to elucidate the overlapping of insulin-like growth factor 1 and FSH in the granulosa mitogenic response.

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