32 research outputs found
Inducible factors for cancer-associated fibroblasts in liver cancer versus myofibroblasts in inflammatory liver disease
The importance of cancer-associated
fibroblasts (CAFs) in liver cancer, cholangiocarcinoma
(CC) and hepatocellular carcinoma (HCC), has been
appreciated in the past 5 years. We focused on how they
get activated in the tumor microenvironment in this
review. Not only hepatic stellate cells (HSCs) but also
portal fibroblasts (PFs) have been appreciated to be key
players in liver fibrogenesis, and their different roles
have just started to be recognized. Since the role of
cholangiocyte in biliary fibrogenic disease might have
some similarities to that of CC, we focused on the role of
cholangiocytes activating stromal fibroblasts, which
would presumably be helpful for better understanding
the mechanism of tumor-CAFs interaction. In addition,
the activation of CAFs should be different from that of
CAFs in HCC, which we consider to be potentially
similar to MFs in hepatocyte injury-dependent liver
fibrogesis. Herein, we describe the activation of CAFs in
CC in comparison to MFs seen in other liver diseases
such as 1) MFs in liver fibrosis caused by hepatocyte
injury such as alcoholic hepatitis, viral hepatitis, and
nonalcoholic steatosis, 2) MFs in liver fibrosis caused by
cholestatic disease, and 3) CAFs in hepatocellular
carcinoma (HCC). This review on the activation of
fibroblasts either in liver cancer or in chronic liver
disease would contribute to CAF-targeted therapy in
liver cancer
Epithelial-mesenchymal transition in gastroenterological cancer
Epithelial-mesenchymal transition (EMT) was first reported as an essential process in embryonic cells and later showed that cancer cells, regardless of the context, exhibit a similar phenomenonthat is crucial for tumor progression. Epithelial cells lose their adhesive characteristic capacity which is necessary for their functions but gain a mesenchymal phenotype. This change from epithelial to mesenchymal phenotype of cancer cells makes it difficult tounderstand the mechanism underlying cancer biology and tumor progression. A number of transcription factors involved in tumor cell EMT and miRNA-regulated EMT have been reported. This review discussed recent findings and new players in EMT in gastrointestinal cancers. Since the molecular mechanisms of tumor progression are sometimes context dependent, the recent findings of EMT have been reviewed in the context-dependent manner