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iNature pancreatic cancer is one of the most deadly malignant tumors in the world, and pancreatic ductal adenocarcinoma (PDAC) is the most common type.
Remodeling of the extracellular matrix (ECM) of distant organs is essential for tumor metastasis, and cancer-derived exosomes can mediate the communication between primary tumor cells and the ECM microenvironment of distant organs.
However, the molecular mechanism process of the liver fibrosis microenvironment has not yet been elucidated.
On April 7, 2021, Shanghai Jiao Tong University Li Qingfeng, Zhang Yi-Fan and Fudan University Fu Deliang jointly published an online publication titled "Exosome-delivered CD44v6/C1QBP complex drives pancreatic cancer liver metastasis by promoting fibrotic" in Gut (IF=19.
82) Liver microenvironment" research paper, which aims to explore the potential mechanism of how PDAC-derived exosomes (Pex) regulate the liver microenvironment and promote metastasis.
Tail vein injection of Pex induces the deposition of extracellular matrix of liver fibrosis, thereby promoting liver metastasis of PDAC.
Specifically, the delivery of the exosomal CD44v6/C1QBP complex to the plasma membrane of hepatic satellite cells (HSC) leads to the phosphorylation of insulin-like growth factor 1 signaling molecules, which leads to HSC activation and liver fibrosis.
The expression of Pex CD44v6 and C1QBP in PDAC patients with liver metastasis was significantly higher than that in PDAC patients without liver metastasis.
At the same time, the high expression of exosomal CD44v6 and C1QBP was associated with a worse prognosis and a higher risk of postoperative PDAC liver metastasis.
In conclusion, the Pex-derived CD44v6/C1QBP complex is essential for the formation of fibrotic liver microenvironment and PDAC liver metastasis.
CD44v6 and C1QBP, which are highly expressed exosomes, are promising biomarkers that can predict the prognosis and liver metastasis of PDAC patients.
Pancreatic cancer is one of the most deadly malignant tumors in the world, and pancreatic ductal adenocarcinoma (PDAC) is the most common type.
At the first diagnosis, distant metastases were detected in more than 80% of PDAC patients, with the liver being the most common metastatic organ.
At present, the treatment options for liver metastasis of PDAC are limited, leading to a higher mortality rate.
This defect is mainly due to insufficient understanding of the underlying mechanism of liver metastasis.
New evidence regarding metastasis indicates that the primary tumor reshapes the microenvironment of future metastatic sites that support tumor growth.
The remodeling of the extracellular matrix (ECM), an important component of the organ microenvironment, in distant organs establishes a pre-metastasis niche that is essential for metastasis.
Circulating tumor cells adhering to the fibrotic ECM can be activated to proliferate.
Immune cells partially remodel the ECM and eventually recruit metastatic cells to specific organs.
In addition, cancer-associated fibroblasts (CAF) in the niche deposit matrix protein before metastasis provide a good fibrotic environment for the arrival of tumor cells.
Although there is research knowledge about the regulation of the liver microenvironment to assist the metastasis process, the molecular mechanism of the microenvironment control of liver fibrosis is still unclear.
Exosomes are extracellular nano-sized (30–150 nm) polymorphic vesicles secreted by all cell types, containing specific proteins, lipids and genetic material.
Tumor cells use this intercellular communication to reprogram target cells and trigger pathological processes related to cancer, such as angiogenesis, immune regulation, and metastasis.
More importantly, the intercellular communication between the original tumor cells and the distant organs through exosomes is essential for the formation and metastasis of the microenvironment before metastasis.
The epidermal growth factor receptor-containing exosomes derived from gastric cancer cells can be delivered to liver stromal cells, and can promote the development of a liver-like microenvironment to promote liver-specific metastasis.
Similarly, the uptake of breast cancer exosomes by lung fibroblasts promotes its activation and fibronectin secretion.
In addition, exosomal small nuclear RNA derived from primary tumors enhanced the expression of matrix metalloproteinases and fibronectin in lung ECM, thereby promoting the formation of niche before metastasis.
Current literature shows that ECM remodeling of distant organs is essential for tumor metastasis, and cancer-derived exosomes can mediate the communication between primary tumor cells and the ECM microenvironment of distant organs.
However, the molecular mechanism process of the microenvironment of liver fibrosis has not been clarified yet.
This study aims to explore the potential mechanism of how PDAC-derived exosomes (Pex) regulate the liver microenvironment and promote metastasis.
Pex tail vein injection induces the deposition of extracellular matrix of liver fibrosis, thereby promoting liver metastasis of PDAC.
Specifically, the delivery of the exosomal CD44v6/C1QBP complex to the plasma membrane of hepatic satellite cells (HSC) leads to the phosphorylation of insulin-like growth factor 1 signaling molecules, which leads to HSC activation and liver fibrosis.
The expression of Pex CD44v6 and C1QBP in PDAC patients with liver metastasis was significantly higher than that in PDAC patients without liver metastasis.
At the same time, the high expression of exosomal CD44v6 and C1QBP was associated with a worse prognosis and a higher risk of postoperative PDAC liver metastasis.
In conclusion, the Pex-derived CD44v6/C1QBP complex is essential for the formation of fibrotic liver microenvironment and PDAC liver metastasis.
CD44v6 and C1QBP, which are highly expressed exosomes, are promising biomarkers that can predict the prognosis and liver metastasis of PDAC patients.
Reference message: https://gut.
bmj.
com/content/early/2021/04/06/gutjnl-2020-323014
Remodeling of the extracellular matrix (ECM) of distant organs is essential for tumor metastasis, and cancer-derived exosomes can mediate the communication between primary tumor cells and the ECM microenvironment of distant organs.
However, the molecular mechanism process of the liver fibrosis microenvironment has not yet been elucidated.
On April 7, 2021, Shanghai Jiao Tong University Li Qingfeng, Zhang Yi-Fan and Fudan University Fu Deliang jointly published an online publication titled "Exosome-delivered CD44v6/C1QBP complex drives pancreatic cancer liver metastasis by promoting fibrotic" in Gut (IF=19.
82) Liver microenvironment" research paper, which aims to explore the potential mechanism of how PDAC-derived exosomes (Pex) regulate the liver microenvironment and promote metastasis.
Tail vein injection of Pex induces the deposition of extracellular matrix of liver fibrosis, thereby promoting liver metastasis of PDAC.
Specifically, the delivery of the exosomal CD44v6/C1QBP complex to the plasma membrane of hepatic satellite cells (HSC) leads to the phosphorylation of insulin-like growth factor 1 signaling molecules, which leads to HSC activation and liver fibrosis.
The expression of Pex CD44v6 and C1QBP in PDAC patients with liver metastasis was significantly higher than that in PDAC patients without liver metastasis.
At the same time, the high expression of exosomal CD44v6 and C1QBP was associated with a worse prognosis and a higher risk of postoperative PDAC liver metastasis.
In conclusion, the Pex-derived CD44v6/C1QBP complex is essential for the formation of fibrotic liver microenvironment and PDAC liver metastasis.
CD44v6 and C1QBP, which are highly expressed exosomes, are promising biomarkers that can predict the prognosis and liver metastasis of PDAC patients.
Pancreatic cancer is one of the most deadly malignant tumors in the world, and pancreatic ductal adenocarcinoma (PDAC) is the most common type.
At the first diagnosis, distant metastases were detected in more than 80% of PDAC patients, with the liver being the most common metastatic organ.
At present, the treatment options for liver metastasis of PDAC are limited, leading to a higher mortality rate.
This defect is mainly due to insufficient understanding of the underlying mechanism of liver metastasis.
New evidence regarding metastasis indicates that the primary tumor reshapes the microenvironment of future metastatic sites that support tumor growth.
The remodeling of the extracellular matrix (ECM), an important component of the organ microenvironment, in distant organs establishes a pre-metastasis niche that is essential for metastasis.
Circulating tumor cells adhering to the fibrotic ECM can be activated to proliferate.
Immune cells partially remodel the ECM and eventually recruit metastatic cells to specific organs.
In addition, cancer-associated fibroblasts (CAF) in the niche deposit matrix protein before metastasis provide a good fibrotic environment for the arrival of tumor cells.
Although there is research knowledge about the regulation of the liver microenvironment to assist the metastasis process, the molecular mechanism of the microenvironment control of liver fibrosis is still unclear.
Exosomes are extracellular nano-sized (30–150 nm) polymorphic vesicles secreted by all cell types, containing specific proteins, lipids and genetic material.
Tumor cells use this intercellular communication to reprogram target cells and trigger pathological processes related to cancer, such as angiogenesis, immune regulation, and metastasis.
More importantly, the intercellular communication between the original tumor cells and the distant organs through exosomes is essential for the formation and metastasis of the microenvironment before metastasis.
The epidermal growth factor receptor-containing exosomes derived from gastric cancer cells can be delivered to liver stromal cells, and can promote the development of a liver-like microenvironment to promote liver-specific metastasis.
Similarly, the uptake of breast cancer exosomes by lung fibroblasts promotes its activation and fibronectin secretion.
In addition, exosomal small nuclear RNA derived from primary tumors enhanced the expression of matrix metalloproteinases and fibronectin in lung ECM, thereby promoting the formation of niche before metastasis.
Current literature shows that ECM remodeling of distant organs is essential for tumor metastasis, and cancer-derived exosomes can mediate the communication between primary tumor cells and the ECM microenvironment of distant organs.
However, the molecular mechanism process of the microenvironment of liver fibrosis has not been clarified yet.
This study aims to explore the potential mechanism of how PDAC-derived exosomes (Pex) regulate the liver microenvironment and promote metastasis.
Pex tail vein injection induces the deposition of extracellular matrix of liver fibrosis, thereby promoting liver metastasis of PDAC.
Specifically, the delivery of the exosomal CD44v6/C1QBP complex to the plasma membrane of hepatic satellite cells (HSC) leads to the phosphorylation of insulin-like growth factor 1 signaling molecules, which leads to HSC activation and liver fibrosis.
The expression of Pex CD44v6 and C1QBP in PDAC patients with liver metastasis was significantly higher than that in PDAC patients without liver metastasis.
At the same time, the high expression of exosomal CD44v6 and C1QBP was associated with a worse prognosis and a higher risk of postoperative PDAC liver metastasis.
In conclusion, the Pex-derived CD44v6/C1QBP complex is essential for the formation of fibrotic liver microenvironment and PDAC liver metastasis.
CD44v6 and C1QBP, which are highly expressed exosomes, are promising biomarkers that can predict the prognosis and liver metastasis of PDAC patients.
Reference message: https://gut.
bmj.
com/content/early/2021/04/06/gutjnl-2020-323014
