Intravasation: Difference between revisions
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{{short description|Invasion of cancer cells into a blood or lymphatic vessel}} |
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'''Intravasation''' |
'''Intravasation''' is the invasion of cancer cells through the [[basement membrane]] into a blood or lymphatic vessel.<ref name="Citation 1">{{cite journal|last=Tsuji|first=Takanori |author2=Soichiro Ibaragi |author3=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|pmid=19738043 |pmc=2760965}}<!--|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|doi=10.1080/15216540701201033|pmid=17454296|s2cid=22158818}}</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 |
==Contributing factors== |
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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.<ref name="Citation 3">{{cite journal|last=Iizumi|first=Megumi| |
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.<ref name="Citation 3">{{cite journal|last=Iizumi|first=Megumi|author2=Wen Liu |author3=Sudha K Pai |author4=Eiji Furuta |author5=Kounosuke Watabe |title=Drug Development Against Metastasis-related Genes and Their Pathways: a Rationale for Cancer Therapy|journal=Biochimica et Biophysica Acta (BBA) - Reviews on Cancer|date=December 2008|volume=1786|issue=2|pages=87–104 |doi=10.1016/j.bbcan.2008.07.002 |pmid=18692117 |pmc=2645343}}</ref> uPA also activates multiple growth factors and [[matrix metalloproteinases]] (MMPs) that further contribute to ECM degradation, thus enabling tumor cell invasion and intravasation.<ref name="Citation 3"/> |
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A newly identified [[metastasis]] suppressor, p75 neurotrophin receptor (p75NTR), is |
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 |
[[Tumor-associated macrophage]]s (TAMs) have been shown to be abundantly present in the microenvironments of metastasizing tumors.<ref name="Citation 4">{{cite journal|last=Condeelis|first=John|author2=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|pmid=16439202|doi-access=free}}<!--|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|pmid=18467655|pmc=2516896}}</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|author2=Georg Krupitza |author3=Wolfgang Mikulits |title=Initial Steps of Metastasis: Cell Invasion and Endothelial Transmigration|journal=Mutation Research|date=October 2011|volume=728|issue=1–2|pages=23–34|doi=10.1016/j.mrrev.2011.05.002|pmid=21605699|pmc=4028085}}</ref> |
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Groups of three cell types (a macrophage, an [[endothelial cell]], and a tumor cell) collectively known as [[tumor microenvironment of metastasis]] (TMEM) can allow tumor cells to enter blood vessels.<ref>{{cite journal |title=Tumor microenvironment of metastasis and risk of distant metastasis of breast cancer |author=Rohan|display-authors=etal |year=2014 |journal=J Natl Cancer Inst |volume=106 |issue=8 |doi=10.1093/jnci/dju136 |pmid=24895374 |pmc=4133559 }}</ref><ref>{{cite web |url=http://www.oncologynurseadvisor.com/web-exclusives/researchers-identify-tumor-microenvironment-of-metastasis-tmem-that-allows-breast-cancer-to-metastasize/article/435246/ |title=Researchers identify tumor microenvironment of metastasis (TMEM) that allows breast cancer to metastasize |author=Boltz |year=2015 }}</ref><ref>{{cite journal |title=Neoadjuvant chemotherapy induces breast cancer metastasis through a TMEM-mediated mechanism |journal=Science Translational Medicine |volume=9 |issue=397 |pages=eaan0026 |doi=10.1126/scitranslmed.aan0026 |pmid=28679654 |pmc=5592784 |author=Karagiannis|display-authors=etal |year=2017 }}</ref> |
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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| |
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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"/> |
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| ⚫ | Tumors can use both active and passive methods to enter the vasculature.<ref name="Citation 7">{{cite journal|last=Bockhorn|first=Maximilian|author2=Rakesh K Jain |author3=Lance L. Munn |title=Active Versus Passive Mechanisms in Metastasis: Do Cancer Cells Crawl into Vessels, or Are They Pushed?|journal=The Lancet Oncology|date=May 2007|volume=8|issue=5|pages=444–448|doi=10.1016/S1470-2045(07)70140-7|pmid=17466902|pmc=2712886}}<!--|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 its early stages is more of a random behavior.<ref name="Citation 8">{{cite journal|last=Cavallaro|first=U|author2=G. Christofori|title=Cell Adhesion in Tumor Invasion and Metastasis: Loss of the Glue is Not Enough|journal=Biochimica et Biophysica Acta (BBA) - Reviews on Cancer|date=30 November 2001|volume=1552|issue=1|pages=39–45|doi=10.1016/s0304-419x(01)00038-5|pmid=11781114}}<!--|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 venous 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|date=August 1993|volume=4|issue=4|pages=219–229|pmid=8400144}}</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 (tissue)|stroma]] and subsequent growth at the secondary site of colonization.<ref name="Citation 9"/> |
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Passive intravasation refers to a process in which tumors metastasize through passive shedding.<ref name="Citation 7"/> Evidence for this is seen when the number of tumor cells released into the circulation increases when the primary tumor experiences trauma.<ref name="Citation 10">{{cite journal|last1=Liotta|first1=L A|last2=Saidel |first2=M G |last3=Kleinerman |first3=J |title=The Significance of Hematogenous Tumor Cell Clumps in the Metastastic Process |url=http://cancerres.aacrjournals.org/content/36/3/889 |journal=Cancer Research|date=March 1976|volume=36|issue=3|pages=889–894|pmid=1253177}}</ref> Cells growing in restricted spaces have been shown to push against each other, causing blood and lymphatic vessels to flatten, potentially forcing cells into the vessels.<ref name="Citation 7"/> |
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==Epithelial-mesenchymal transition and Intravasation== |
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==Epithelial–mesenchymal transition and intravasation== |
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| ⚫ | [[Epithelial–mesenchymal transition]] (EMT) has been hypothesized to be an absolute requirement for tumor invasion and metastasis,<ref name="Citation 1"/> although both EMT and non-EMT{{clarify|date=March 2023}} cells have been shown to cooperate to complete the spontaneous metastasis process.<ref name="Citation 1"/> EMT cells with migratory phenotype degrade the ECM and penetrate local tissue and blood or lymphatic vessels, thereby facilitating intravasation.<ref name="Citation 1"/> Non-EMT cells can migrate together with EMT cells to enter the blood or lymphatic vessels.<ref name="Citation 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.<ref name="Citation 1"/> |
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==References== |
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{{Reflist}} |
{{Reflist}} |
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[[Category:Oncology]] |
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{{Uncategorized|date=April 2012}} |
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Latest revision as of 14:43, 18 March 2023
Intravasation is the invasion of cancer cells through the basement 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
[edit]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]
Groups of three cell types (a macrophage, an endothelial cell, and a tumor cell) collectively known as tumor microenvironment of metastasis (TMEM) can allow tumor cells to enter blood vessels.[7][8][9]
Active and passive intravasation
[edit]Tumors can use both active and passive methods to enter the vasculature.[10] 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 its early stages is more of a random behavior.[11]
In active intravasation, cancerous cells actively migrate toward and then into nearby blood vessels.[10] The first step in this process is specific adhesion to venous endothelial cells, followed by adherence to proteins of the subendothelial basement membrane, such as laminin and types IV and V collagen.[12] 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.[12]
Passive intravasation refers to a process in which tumors metastasize through passive shedding.[10] Evidence for this is seen when the number of tumor cells released into the circulation increases when the primary tumor experiences trauma.[13] Cells growing in restricted spaces have been shown to push against each other, causing blood and lymphatic vessels to flatten, potentially forcing cells into the vessels.[10]
Epithelial–mesenchymal transition and intravasation
[edit]Epithelial–mesenchymal transition (EMT) has been hypothesized to be an absolute requirement for tumor invasion and metastasis,[1] although both EMT and non-EMT[clarification needed] 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
[edit]- ^ a b c d e f Tsuji, Takanori; Soichiro Ibaragi; Guo-Fu Hu (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. PMC 2760965. PMID 19738043.
- ^ a b c Soon, Lilian (2007). "A Discourse on Cancer Cell Chemotaxis: Where to from Here?". IUBMB Life. 59 (2): 60–67. doi:10.1080/15216540701201033. PMID 17454296. S2CID 22158818.
- ^ a b c Iizumi, Megumi; Wen Liu; Sudha K Pai; Eiji Furuta; Kounosuke Watabe (December 2008). "Drug Development Against Metastasis-related Genes and Their Pathways: a Rationale for Cancer Therapy". Biochimica et Biophysica Acta (BBA) - Reviews on Cancer. 1786 (2): 87–104. doi:10.1016/j.bbcan.2008.07.002. PMC 2645343. PMID 18692117.
- ^ Condeelis, John; Jeffrey W. Pollard (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. PMID 16439202.
- ^ 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. PMC 2516896. PMID 18467655.
- ^ a b van Zijil, Franziska; Georg Krupitza; Wolfgang Mikulits (October 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. PMC 4028085. PMID 21605699.
- ^ Rohan; et al. (2014). "Tumor microenvironment of metastasis and risk of distant metastasis of breast cancer". J Natl Cancer Inst. 106 (8). doi:10.1093/jnci/dju136. PMC 4133559. PMID 24895374.
- ^ Boltz (2015). "Researchers identify tumor microenvironment of metastasis (TMEM) that allows breast cancer to metastasize".
- ^ Karagiannis; et al. (2017). "Neoadjuvant chemotherapy induces breast cancer metastasis through a TMEM-mediated mechanism". Science Translational Medicine. 9 (397): eaan0026. doi:10.1126/scitranslmed.aan0026. PMC 5592784. PMID 28679654.
- ^ a b c d Bockhorn, Maximilian; Rakesh K Jain; Lance L. Munn (May 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. PMC 2712886. PMID 17466902.
- ^ Cavallaro, U; G. Christofori (30 November 2001). "Cell Adhesion in Tumor Invasion and Metastasis: Loss of the Glue is Not Enough". Biochimica et Biophysica Acta (BBA) - Reviews on Cancer. 1552 (1): 39–45. doi:10.1016/s0304-419x(01)00038-5. PMID 11781114.
- ^ a b Zetter, B R. (August 1993). "Adhesion Molecules in Tumor Metastasis". Seminars in Cancer Biology. 4 (4): 219–229. PMID 8400144.
- ^ Liotta, L A; Saidel, M G; Kleinerman, J (March 1976). "The Significance of Hematogenous Tumor Cell Clumps in the Metastastic Process". Cancer Research. 36 (3): 889–894. PMID 1253177.