Intravasation: Difference between revisions
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'''Intravasation''' refers to the invasion of cancer cells through the [[basal membrane]] into a blood or lymphatic vessel.<ref name="Citation 1">{{cite journal|last=Tsuji|first=Takanori|coauthors=Soichiro Ibaragi, Guo-Fu Hu|title=Epithelial-Mesenchymal Transition and Cell Cooperativity in Metastasis|journal=Cancer Research|date=15 |
'''Intravasation''' refers to the invasion of cancer cells through the [[basal membrane]] into a blood or lymphatic vessel.<ref name="Citation 1">{{cite journal|last=Tsuji|first=Takanori|coauthors=Soichiro Ibaragi, Guo-Fu Hu|title=Epithelial-Mesenchymal Transition and Cell Cooperativity in Metastasis|journal=Cancer Research|date=15 September 2009|volume=69|issue=18|pages=7135–7139|doi=10.1158/0008-5472.CAN-09-1618|accessdate=15 April 2012}}</ref> Intravasation is one of several carcinogenic events that initiate the escape of cancerous cells from their primary sites.<ref name="Citation 2">{{cite journal|last=Soon|first=Lilian|title=A Discourse on Cancer Cell Chemotaxis: Where to from Here?|journal=IUBMB Life|year=2007|volume=59|issue=2|pages=60–67}}</ref> Other mechanisms include invasion through [[basement membranes]], [[extravasation]], and colonization of distant metastatic sites.<ref name="Citation 2"/> Cancer cell [[chemotaxis]] also relies on this migratory behavior to arrive at a secondary destination designated for cancer cell colonization.<ref name="Citation 2"/> |
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==Contributing factors== |
==Contributing factors== |
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A newly identified [[metastasis]] suppressor, p75 neurotrophin receptor (p75NTR), is able to suppress metastasis in part by causing specific proteases, such as uPA, to be downregulated.<ref name="Citation 3"/> |
A newly identified [[metastasis]] suppressor, p75 neurotrophin receptor (p75NTR), is able to suppress metastasis in part by causing specific proteases, such as uPA, to be downregulated.<ref name="Citation 3"/> |
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Tumor associated macrophages (TAMs) have been shown to be abundantly present in the microenvironments of metastasizing tumors.<ref name="Citation 4">{{cite journal|last=Condeelis|first=John|coauthors=Jeffrey W. Pollard|title=Macrophages: Obligate Partners for Tumor Cell Migration, Invasion, and Metastasis|journal=Cell|date=27 |
Tumor associated macrophages (TAMs) have been shown to be abundantly present in the microenvironments of metastasizing tumors.<ref name="Citation 4">{{cite journal|last=Condeelis|first=John|coauthors=Jeffrey W. Pollard|title=Macrophages: Obligate Partners for Tumor Cell Migration, Invasion, and Metastasis|journal=Cell|date=27 January 2006|volume=124|issue=2|pages=263–266|doi=10.1016/j.cell.2006.01.007|accessdate=15 April 2012}}</ref><ref name="Citation 5">{{cite journal|last=Pollard|first=Jeffrey W.|title=Macrophages Define the Invasive Microenvironment in Breast Cancer|journal=Journal of Leukocyte Biology|date=1 September 2008|volume=84|issue=3|pages=623–630|doi=10.1189/jlb.1107762}}</ref> Studies have revealed that macrophages enhance tumor cell migration and intravasation by secreting chemotactic and chemokinetic factors, promoting angiogenesis, remodeling the ECM, and regulating the formation of collagen fibers.<ref name="Citation 5"/><ref name="Citation 6">{{cite journal|last=van Zijil|first=Franziska|coauthors=Georg Krupitza, Wolfgang Mikulits|title=Initial Steps of Metastasis: Cell Invasion and Endothelial Transmigration|journal=Mutation Research|year=2011|month=October|volume=728|issue=1-2|pages=23–34|doi=10.1016/j.mrrev.2011.05.002}}</ref> |
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==Active and passive intravasation== |
==Active and passive intravasation== |
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Tumors can use both active and passive methods to enter vasculature.<ref name="Citation 7">{{cite journal|last=Bockhorn|first=Maximilian|coauthors=Rakesh K Jain, Lance L. Munn|title=Active Versus Passive Mechanisms in Metastasis: Do Cancer Cells Crawl into Vessels, or Are They Pushed?|journal=The Lancet Oncology|year=2007|month=Msy|volume=8|issue=5|pages=444–448|doi=10.1016/S1470-2045(07)70140-7|accessdate=15 April 2012}}</ref> Some studies suggest that cancer cells actively move towards blood or lymphatic vessels in response to nutrient or chemokine gradients,<ref name="Citation 6"/> while others provide evidence for the hypothesis that metastasis in the early stages is more accidental.<ref name="Citation 8">{{cite journal|last=Cavallaro|first=U|coauthors=G. Christofori|title=Cell Adhesion in Tumor Invasion and Metastasis: Loss of the Glue is Not Enough|journal=Biochimica Et Biophysica Acta|date=30 |
Tumors can use both active and passive methods to enter vasculature.<ref name="Citation 7">{{cite journal|last=Bockhorn|first=Maximilian|coauthors=Rakesh K Jain, Lance L. Munn|title=Active Versus Passive Mechanisms in Metastasis: Do Cancer Cells Crawl into Vessels, or Are They Pushed?|journal=The Lancet Oncology|year=2007|month=Msy|volume=8|issue=5|pages=444–448|doi=10.1016/S1470-2045(07)70140-7|accessdate=15 April 2012}}</ref> Some studies suggest that cancer cells actively move towards blood or lymphatic vessels in response to nutrient or chemokine gradients,<ref name="Citation 6"/> while others provide evidence for the hypothesis that metastasis in the early stages is more accidental.<ref name="Citation 8">{{cite journal|last=Cavallaro|first=U|coauthors=G. Christofori|title=Cell Adhesion in Tumor Invasion and Metastasis: Loss of the Glue is Not Enough|journal=Biochimica Et Biophysica Acta|date=30 November 2001|volume=1552|issue=1|pages=39–45|accessdate=15 April 2012}}</ref> |
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In active intravasation, cancerous cells actively migrate toward and then into nearby blood vessels.<ref name="Citation 7"/> The first step in this process is specific adhesion to venular endothelial cells, followed by adherence to proteins of the subendothelial basement membrane, such as [[laminin]] and types IV and V [[collagen]].<ref name="Citation 9">{{cite journal|last=Zetter|first=B R.|title=Adhesion Molecules in Tumor Metastasis|journal=Seminars in Cancer Biology|year=1993|month=August|volume=4|issue=4|pages=219–229}}</ref> The final step is the adhesion of the metastatic tumor cell to connective tissue elements such as [[fibronectin]], [[type I collagen]], and [[hyaluronan]], which is required for the movement of the tumor cell into the subendothelial stroma and subsequent growth at the secondary site of colonization.<ref name="Citation 9"/> |
In active intravasation, cancerous cells actively migrate toward and then into nearby blood vessels.<ref name="Citation 7"/> The first step in this process is specific adhesion to venular endothelial cells, followed by adherence to proteins of the subendothelial basement membrane, such as [[laminin]] and types IV and V [[collagen]].<ref name="Citation 9">{{cite journal|last=Zetter|first=B R.|title=Adhesion Molecules in Tumor Metastasis|journal=Seminars in Cancer Biology|year=1993|month=August|volume=4|issue=4|pages=219–229}}</ref> The final step is the adhesion of the metastatic tumor cell to connective tissue elements such as [[fibronectin]], [[type I collagen]], and [[hyaluronan]], which is required for the movement of the tumor cell into the subendothelial stroma and subsequent growth at the secondary site of colonization.<ref name="Citation 9"/> |
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Revision as of 02:53, 25 December 2013
Intravasation refers to the invasion of cancer cells through the basal membrane into a blood or lymphatic vessel.[1] Intravasation is one of several carcinogenic events that initiate the escape of cancerous cells from their primary sites.[2] Other mechanisms include invasion through basement membranes, extravasation, and colonization of distant metastatic sites.[2] Cancer cell chemotaxis also relies on this migratory behavior to arrive at a secondary destination designated for cancer cell colonization.[2]
Contributing factors
One of the genes that contributes to intravasation codes for urokinase (uPA), a serine protease that is able to proteolytically degrade various extracellular matrix (ECM) components and the basement membrane around primary tumors.[3] uPA also activates multiple growth factors and matrix metalloproteinases (MMPs) that further contribute to ECM degradation, thus enabling tumor cell invasion and intravasation.[3]
A newly identified metastasis suppressor, p75 neurotrophin receptor (p75NTR), is able to suppress metastasis in part by causing specific proteases, such as uPA, to be downregulated.[3]
Tumor associated macrophages (TAMs) have been shown to be abundantly present in the microenvironments of metastasizing tumors.[4][5] Studies have revealed that macrophages enhance tumor cell migration and intravasation by secreting chemotactic and chemokinetic factors, promoting angiogenesis, remodeling the ECM, and regulating the formation of collagen fibers.[5][6]
Active and passive intravasation
Tumors can use both active and passive methods to enter vasculature.[7] Some studies suggest that cancer cells actively move towards blood or lymphatic vessels in response to nutrient or chemokine gradients,[6] while others provide evidence for the hypothesis that metastasis in the early stages is more accidental.[8]
In active intravasation, cancerous cells actively migrate toward and then into nearby blood vessels.[7] The first step in this process is specific adhesion to venular endothelial cells, followed by adherence to proteins of the subendothelial basement membrane, such as laminin and types IV and V collagen.[9] The final step is the adhesion of the metastatic tumor cell to connective tissue elements such as fibronectin, type I collagen, and hyaluronan, which is required for the movement of the tumor cell into the subendothelial stroma and subsequent growth at the secondary site of colonization.[9]
Passive intravasation refers to a process in which tumors metastasize through passive shedding.[7] Evidence for this is seen when the number of tumor cells released into the blood stream increases when the primary tumor experiences trauma.[10] Additionally, cells growing in restricted spaces have been shown to push against each other causing blood and lymphatic vessels to collapse, potentially forcing cells into the vessels.[7]
Epithelial-mesenchymal transition and intravasation
Epithelial-mesenchymal transition (EMT) has been hypothesized to be an absolute requirement for tumor invasion and metastasis.[1] However, both EMT and non-EMT cells have been shown to cooperate to complete the spontaneous metastasis process.[1] EMT cells, with migratory phenotype, degrade the ECM and penetrate local tissue and blood or lymphatic vessels, thereby facilitating intravasation.[1] Non-EMT cells can migrate together with EMT cells to enter the blood or lymphatic vessels.[1] Although both cell types persist in circulation, EMT cells fail to adhere to the vessel wall at the secondary site, while non-EMT cells, which have greater adhesive properties, are able to attach to the vessel wall and extravasate into the secondary site.[1]
References
- ^ a b c d e f Tsuji, Takanori (15 September 2009). "Epithelial-Mesenchymal Transition and Cell Cooperativity in Metastasis". Cancer Research. 69 (18): 7135–7139. doi:10.1158/0008-5472.CAN-09-1618.
{{cite journal}}:|access-date=requires|url=(help); Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ a b c Soon, Lilian (2007). "A Discourse on Cancer Cell Chemotaxis: Where to from Here?". IUBMB Life. 59 (2): 60–67.
- ^ a b c Iizumi, Megumi (2008). "Drug Development Against Metastasis-related Genes and Their Pathways: a Rationale for Cancer Therapy". Biochimica Et Biophysica Acta. 1786 (2): 87–104.
{{cite journal}}: Unknown parameter|coauthors=ignored (|author=suggested) (help); Unknown parameter|month=ignored (help) - ^ Condeelis, John (27 January 2006). "Macrophages: Obligate Partners for Tumor Cell Migration, Invasion, and Metastasis". Cell. 124 (2): 263–266. doi:10.1016/j.cell.2006.01.007.
{{cite journal}}:|access-date=requires|url=(help); Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ a b Pollard, Jeffrey W. (1 September 2008). "Macrophages Define the Invasive Microenvironment in Breast Cancer". Journal of Leukocyte Biology. 84 (3): 623–630. doi:10.1189/jlb.1107762.
- ^ a b van Zijil, Franziska (2011). "Initial Steps of Metastasis: Cell Invasion and Endothelial Transmigration". Mutation Research. 728 (1–2): 23–34. doi:10.1016/j.mrrev.2011.05.002.
{{cite journal}}: Unknown parameter|coauthors=ignored (|author=suggested) (help); Unknown parameter|month=ignored (help) - ^ a b c d Bockhorn, Maximilian (2007). "Active Versus Passive Mechanisms in Metastasis: Do Cancer Cells Crawl into Vessels, or Are They Pushed?". The Lancet Oncology. 8 (5): 444–448. doi:10.1016/S1470-2045(07)70140-7.
{{cite journal}}:|access-date=requires|url=(help); Unknown parameter|coauthors=ignored (|author=suggested) (help); Unknown parameter|month=ignored (help) - ^ Cavallaro, U (30 November 2001). "Cell Adhesion in Tumor Invasion and Metastasis: Loss of the Glue is Not Enough". Biochimica Et Biophysica Acta. 1552 (1): 39–45.
{{cite journal}}:|access-date=requires|url=(help); Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ a b Zetter, B R. (1993). "Adhesion Molecules in Tumor Metastasis". Seminars in Cancer Biology. 4 (4): 219–229.
{{cite journal}}: Unknown parameter|month=ignored (help) - ^ Liotta, L A. "The Significane of Hematogenous Tumor Cell Clumps in the Metastastic Process". Cancer Research. 36 (3): 889–894.
{{cite journal}}: Unknown parameter|coauthors=ignored (|author=suggested) (help); Unknown parameter|month=ignored (help)