Development of a three-dimensional culture model of prostatic epithelial cells and its use for the study of epithelial-mesenchymal transition and inhibition of PI3K pathway in prostate cancer

The Prostate ◽  
2008 ◽  
Vol 69 (4) ◽  
pp. 428-442 ◽  
Author(s):  
Jian Hong Chu ◽  
Shan Yu ◽  
Simon W. Hayward ◽  
Franky L. Chan
Keyword(s):  
Prostate Cancer ◽  
Epithelial Cells ◽  
Epithelial Mesenchymal Transition ◽  
Three Dimensional ◽  
Pi3k Pathway ◽  
Mesenchymal Transition ◽  
Culture Model ◽  
Three Dimensional Culture

scholarly journals Slug Is Required for Cell Survival during Partial Epithelial-Mesenchymal Transition of HGF-induced Tubulogenesis

2007 ◽  
Vol 18 (5) ◽  
pp. 1943-1952 ◽  
Author(s):  
Pascale Leroy ◽  
Keith E. Mostov
Keyword(s):  
Transcription Factors ◽  
Cell Survival ◽  
Epithelial Mesenchymal Transition ◽  
Three Dimensional ◽  
Cell Movement ◽  
Mesenchymal Transition ◽  
Culture Model ◽  
Snail Family ◽  
Hepatocyte Growth ◽  
Darby Canine Kidney

Transcription factors of the Snail family are key regulators of epithelial-mesenchymal transition (EMT). In many processes during development or disease, cells do not acquire all the characteristics associated with EMT, leading to what we refer to as partial EMT (p-EMT). However, little is known of the implications of the Snail transcription factors in processes that only involve a p-EMT. To assess this, we used the hepatocyte growth factor (HGF)-induced Madin-Darby canine kidney tubulogenesis system, which provides a three-dimensional culture model of a morphogenetic process including a p-EMT. We found that although Slug (Snail2) is highly and transitory up-regulated during the p-EMT phase of tubulogenesis, it is not a repressor of E-cadherin during this process. Using inducible knockdown of Slug, we demonstrate that Slug is not an inducer of cell movement and instead is required for survival during p-EMT. We conclude that in epithelial cells, promoting cell survival can be a primary function of Slug, rather than being acquired concomitantly with EMT.

scholarly journals Signaling Pathways Induced by Leptin during Epithelial–Mesenchymal Transition in Breast Cancer

2018 ◽  
Vol 19 (11) ◽  
pp. 3493 ◽  
Author(s):  
Monserrat Olea-Flores ◽  
Juan Juárez-Cruz ◽  
Miguel Mendoza-Catalán ◽  
Teresita Padilla-Benavides ◽  
Napoleón Navarro-Tito
Keyword(s):  
Breast Cancer ◽  
Extracellular Matrix ◽  
Epithelial Cells ◽  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
Three Dimensional ◽  
Public Health Problem ◽  
Metastatic Carcinoma ◽  
Surrounding Tissue ◽  
Mesenchymal Transition

Leptin is an adipokine that is overexpressed in obese and overweight people. Interestingly, women with breast cancer present high levels of leptin and of its receptor ObR. Leptin plays an important role in breast cancer progression due to the biological processes it participates in, such as epithelial–mesenchymal transition (EMT). EMT consists of a series of orchestrated events in which cell–cell and cell–extracellular matrix interactions are altered and lead to the release of epithelial cells from the surrounding tissue. The cytoskeleton is also re-arranged, allowing the three-dimensional movement of epithelial cells into the extracellular matrix. This transition provides cells with the ability to migrate and invade adjacent or distal tissues, which is a classic feature of invasive or metastatic carcinoma cells. In recent years, the number of cases of breast cancer has increased, making this disease a public health problem worldwide and the leading cause of death due to cancer in women. In this review, we focus on recent advances that establish: (1) leptin as a risk factor for the development of breast cancer, and (2) leptin as an inducer of EMT, an event that promotes tumor progression.

Magnesium Chloride is an Effective Therapeutic Agent for Prostate Cancer

2018 ◽  
Vol 8 (1) ◽  
pp. 62 ◽  
Author(s):  
Julianna Maria Santos ◽  
Fazle Hussain
Keyword(s):  
Prostate Cancer ◽  
Magnesium Chloride ◽  
Epithelial Mesenchymal Transition ◽  
Chromatin Condensation ◽  
Myosin Ii ◽  
In Vivo Studies ◽  
Migration Speed ◽  
Mesenchymal Transition

Background: Reduced levels of magnesium can cause several diseases and increase cancer risk. Motivated by magnesium chloride’s (MgCl2) non-toxicity, physiological importance, and beneficial clinical applications, we studied its action mechanism and possible mechanical, molecular, and physiological effects in prostate cancer with different metastatic potentials.Methods: We examined the effects of MgCl2, after 24 and 48 hours, on apoptosis, cell migration, expression of epithelial mesenchymal transition (EMT) markers, and V-H+-ATPase, myosin II (NMII) and the transcription factor NF Kappa B (NFkB) expressions.Results: MgCl2 induces apoptosis, and significantly decreases migration speed in cancer cells with different metastatic potentials.  MgCl2 reduces the expression of V-H+-ATPase and myosin II that facilitates invasion and metastasis, suppresses the expression of vimentin and increases expression of E-cadherin, suggesting a role of MgCl2 in reversing the EMT. MgCl2 also significantly increases the chromatin condensation and decreases NFkB expression.Conclusions: These results suggest a promising preventive and therapeutic role of MgCl2 for prostate cancer. Further studies should explore extending MgCl2 therapy to in vivo studies and other cancer types.Keywords: Magnesium chloride, prostate cancer, migration speed, V-H+-ATPase, and EMT.

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