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Role of cancer microenvironment in metastasis: focus on colon cancer.

Gout S, Huot J - Cancer Microenviron (2008)

Bottom Line: In most cases, death will result from the formation of distal secondary sites called metastases.These mutations lead to unrestrained growth of the primary neoplasm and a propensity to detach and to progress through the subsequent steps of metastatic dissemination.This process depends tightly on the surrounding microenvironment.

View Article: PubMed Central - PubMed

Affiliation: Le Centre de recherche en cancérologie de l'Université Laval, L'Hôtel-Dieu de Québec, 9 rue McMahon, Quebec, Canada.

ABSTRACT
One person on three will receive a diagnostic of cancer during his life. About one third of them will die of the disease. In most cases, death will result from the formation of distal secondary sites called metastases. Several events that lead to cancer are under genetic control. In particular, cancer initiation is tightly associated with specific mutations that affect proto-oncogenes and tumour suppressor genes. These mutations lead to unrestrained growth of the primary neoplasm and a propensity to detach and to progress through the subsequent steps of metastatic dissemination. This process depends tightly on the surrounding microenvironment. In fact, several studies support the point that tumour development relies on a continuous cross-talk between cancer cells and their cellular and extracellular microenvironments. This signaling cross-talk is mediated by transmembrane receptors expressed on cancer cells and stromal cells. The aim of this manuscript is to review how the cancer microenvironment influences the journey of a metastatic cell taking liver invasion by colorectal cancer cells as a model.

No MeSH data available.


Related in: MedlinePlus

Mechanisms of VEGF-C-induced intravasation of cancer cells across lymph vessels. In several human cancers, increased expression of VEGF-C in primary tumours correlates with regional lymph node metastases. It is possible that a reciprocal cross-talk exists between tumour cells and lymphatic endothelial cells to induce tumour lymphangiogenesis and formation of lymph node metastases. Notably, VEGF-C activates lymphatic endothelial cells (1) that in turn may secrete chemotactic factors (2). This will contribute to attract cancer cells bearing appropriate chemokine receptors to the growing lymph vessels (3), and enable their adhesion and their intra-lymphatic intravasation
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Fig4: Mechanisms of VEGF-C-induced intravasation of cancer cells across lymph vessels. In several human cancers, increased expression of VEGF-C in primary tumours correlates with regional lymph node metastases. It is possible that a reciprocal cross-talk exists between tumour cells and lymphatic endothelial cells to induce tumour lymphangiogenesis and formation of lymph node metastases. Notably, VEGF-C activates lymphatic endothelial cells (1) that in turn may secrete chemotactic factors (2). This will contribute to attract cancer cells bearing appropriate chemokine receptors to the growing lymph vessels (3), and enable their adhesion and their intra-lymphatic intravasation

Mentions: As described in the previous sections, colon cancer cells can also disseminate via the lymphatic vessels, which is supported by the close correlation existing between liver metastasis and lymphangiogenesis. The mechanisms by which lymphangiogenesis contributes to colon cancer and cancer metastasis in general are still unclear. It is possible that VEGF-C stimulated lymphatic endothelial cells secrete chemotactic or mitogenic factors that will attract cancer cells to the newly growing lymph vessels enabling their adhesion and intravasation on and through the lymphatic endothelium [72]. In this context, expression of CXCR4 and CCR7 by human breast cancer cells facilitate their migration to the lymph nodes [95]. Once they have interacted with the endothelium of the lymphangiogenic vessels, the entry of cancer cells in these vessels will be greatly facilitated by the fact that they are leaky and tortuous (Fig. 4). As mentioned earlier, colorectal cancer cells express the CXCR5 chemokine receptor and both lymph endothelial cells and the liver express its ligand BCA-1/CXCL13 [79]. It is, then, possible that cancer cells may be directed via lymphangiogenesis to both lymph nodes and liver.Fig. 4


Role of cancer microenvironment in metastasis: focus on colon cancer.

Gout S, Huot J - Cancer Microenviron (2008)

Mechanisms of VEGF-C-induced intravasation of cancer cells across lymph vessels. In several human cancers, increased expression of VEGF-C in primary tumours correlates with regional lymph node metastases. It is possible that a reciprocal cross-talk exists between tumour cells and lymphatic endothelial cells to induce tumour lymphangiogenesis and formation of lymph node metastases. Notably, VEGF-C activates lymphatic endothelial cells (1) that in turn may secrete chemotactic factors (2). This will contribute to attract cancer cells bearing appropriate chemokine receptors to the growing lymph vessels (3), and enable their adhesion and their intra-lymphatic intravasation
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2654352&req=5

Fig4: Mechanisms of VEGF-C-induced intravasation of cancer cells across lymph vessels. In several human cancers, increased expression of VEGF-C in primary tumours correlates with regional lymph node metastases. It is possible that a reciprocal cross-talk exists between tumour cells and lymphatic endothelial cells to induce tumour lymphangiogenesis and formation of lymph node metastases. Notably, VEGF-C activates lymphatic endothelial cells (1) that in turn may secrete chemotactic factors (2). This will contribute to attract cancer cells bearing appropriate chemokine receptors to the growing lymph vessels (3), and enable their adhesion and their intra-lymphatic intravasation
Mentions: As described in the previous sections, colon cancer cells can also disseminate via the lymphatic vessels, which is supported by the close correlation existing between liver metastasis and lymphangiogenesis. The mechanisms by which lymphangiogenesis contributes to colon cancer and cancer metastasis in general are still unclear. It is possible that VEGF-C stimulated lymphatic endothelial cells secrete chemotactic or mitogenic factors that will attract cancer cells to the newly growing lymph vessels enabling their adhesion and intravasation on and through the lymphatic endothelium [72]. In this context, expression of CXCR4 and CCR7 by human breast cancer cells facilitate their migration to the lymph nodes [95]. Once they have interacted with the endothelium of the lymphangiogenic vessels, the entry of cancer cells in these vessels will be greatly facilitated by the fact that they are leaky and tortuous (Fig. 4). As mentioned earlier, colorectal cancer cells express the CXCR5 chemokine receptor and both lymph endothelial cells and the liver express its ligand BCA-1/CXCL13 [79]. It is, then, possible that cancer cells may be directed via lymphangiogenesis to both lymph nodes and liver.Fig. 4

Bottom Line: In most cases, death will result from the formation of distal secondary sites called metastases.These mutations lead to unrestrained growth of the primary neoplasm and a propensity to detach and to progress through the subsequent steps of metastatic dissemination.This process depends tightly on the surrounding microenvironment.

View Article: PubMed Central - PubMed

Affiliation: Le Centre de recherche en cancérologie de l'Université Laval, L'Hôtel-Dieu de Québec, 9 rue McMahon, Quebec, Canada.

ABSTRACT
One person on three will receive a diagnostic of cancer during his life. About one third of them will die of the disease. In most cases, death will result from the formation of distal secondary sites called metastases. Several events that lead to cancer are under genetic control. In particular, cancer initiation is tightly associated with specific mutations that affect proto-oncogenes and tumour suppressor genes. These mutations lead to unrestrained growth of the primary neoplasm and a propensity to detach and to progress through the subsequent steps of metastatic dissemination. This process depends tightly on the surrounding microenvironment. In fact, several studies support the point that tumour development relies on a continuous cross-talk between cancer cells and their cellular and extracellular microenvironments. This signaling cross-talk is mediated by transmembrane receptors expressed on cancer cells and stromal cells. The aim of this manuscript is to review how the cancer microenvironment influences the journey of a metastatic cell taking liver invasion by colorectal cancer cells as a model.

No MeSH data available.


Related in: MedlinePlus