Stellate Cells (SC) are morphologically characterized by dendrites that radiate from the main cell body leading to a star-like shape and giving rise to the name Stellate i.e. star-like. They can be found in various parts of the body such as: kidneys, lungs, liver, breast, and pancreas; some of these ones have been less thoroughly characterized compared to others such as hepatic SC [1-5]. Although the dissimilar microenvironment of SC in different parts of the body condition them to react different, it have been shown that they have morphological and biochemical similarities. In their quiescent state, they store and transports vitamin A compounds (retinoid) in the form of droplets in their cytoplast. During an injury they undergo structural
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However, the relationship pancreatic cancer- PSC can be described by a pathological feedback loop that is not completely understood. Cancer cells stimulate stellate cells to secrete more vascular endothelial growth factor, but stellate cells contribute to the hypoxia of fibrotic tissue by increasing the endostatin production [11]. Although, several studies confirm that stellate cells contribute to tumor growth and metastasis, it is poorly understood the mechanism by with they do it. There is no evidence that the elimination of PSC mitigates the progression of cancer, yet the modulation of these ones might influence it [12]. Overall, it is uncertainty if SC are really partners in crime or some sort of double agent that also regulates spread of oncogene-initiated epithelium.
My goal is to use a mechanistic approach to explore the apparatus of action of pancreatic stellate cells and the influence of its activation in their microenvironment and cancer cells. Consequently, this knowledge can provide a practical way to find novel therapeutic targets and improve patient’s quality of …show more content…
It has been seen that PSC stimulate the proliferation of cancer cells and vice versa via proteins such as galactin-3, TGF-beta, PDGF, etc; which shows the important role of pancreatic SC in early proliferation of cancer cells [14,15].
Haqq et al. made a great job reviewing current evidence about the mechanism of action of activated pancreatic stellate cells and their interaction with cancer cells. This review paper and a quick google search shows that proliferation is one of the most common parameters measured in both in vitro and in vivo studies of PSC; other subject of study include migration, gene expression, cell signaling, etc.[17]. Yet not many people have look into the mechanical properties of cellular microenvironment by studying the effects of PSC contractility and matrix cross-linking.
Therefore, I plan to tackle this issue by focusing in the role of pancreatic SC contractility and cross-linking capability in their interaction with cancer cells and influence in diseases such as fibrosis, pancreatitis, and
However, the relationship pancreatic cancer- PSC can be described by a pathological feedback loop that is not completely understood. Cancer cells stimulate stellate cells to secrete more vascular endothelial growth factor, but stellate cells contribute to the hypoxia of fibrotic tissue by increasing the endostatin production [11]. Although, several studies confirm that stellate cells contribute to tumor growth and metastasis, it is poorly understood the mechanism by with they do it. There is no evidence that the elimination of PSC mitigates the progression of cancer, yet the modulation of these ones might influence it [12]. Overall, it is uncertainty if SC are really partners in crime or some sort of double agent that also regulates spread of oncogene-initiated epithelium.
My goal is to use a mechanistic approach to explore the apparatus of action of pancreatic stellate cells and the influence of its activation in their microenvironment and cancer cells. Consequently, this knowledge can provide a practical way to find novel therapeutic targets and improve patient’s quality of …show more content…
It has been seen that PSC stimulate the proliferation of cancer cells and vice versa via proteins such as galactin-3, TGF-beta, PDGF, etc; which shows the important role of pancreatic SC in early proliferation of cancer cells [14,15].
Haqq et al. made a great job reviewing current evidence about the mechanism of action of activated pancreatic stellate cells and their interaction with cancer cells. This review paper and a quick google search shows that proliferation is one of the most common parameters measured in both in vitro and in vivo studies of PSC; other subject of study include migration, gene expression, cell signaling, etc.[17]. Yet not many people have look into the mechanical properties of cellular microenvironment by studying the effects of PSC contractility and matrix cross-linking.
Therefore, I plan to tackle this issue by focusing in the role of pancreatic SC contractility and cross-linking capability in their interaction with cancer cells and influence in diseases such as fibrosis, pancreatitis, and