Tumor Self-Seeding by Circulating Cancer Cells

Kim, Mi Young; Oskarsson, Thordur; Acharyya, Swarnali; Nguyen, Don X.; Zhang, Xiang H.-F.; Norton, Larry; Massagué, Joan

doi:10.1016/j.cell.2009.11.025

Cited by 1,173 publications

(964 citation statements)

References 47 publications

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“…This process, which is called tumor self-seeding, can accelerate tumor growth and angiogenesis. CTCs produce ELR-positive CXC chemokines including CXCL8 and CXCL1, and these chemokines eventually promote self-seeding [34].…”

Section: Direct Effects On Cancer Cellsmentioning

confidence: 99%

Chemokines in tumor development and progression

Mukaida

Baba

2012

Experimental Cell Research

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Section: Direct Effects On Cancer Cellsmentioning

confidence: 99%

Chemokines in tumor development and progression

Mukaida

Baba

2012

Experimental Cell Research

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“…NF-κB is itself activated by these same inflammatory cytokines (23,24). The serum levels of cytokines have been reported to be elevated in patients with breast, colorectal and lung cancers (25)(26)(27)(28). IL-6, which has diverse biological effects on immune and inflammatory responses, is produced in response to infection or injury in a variety of cells, including monocytes, lymphocytes, fibroblasts, ECs and keratinocytes.…”

Section: Discussionmentioning

confidence: 99%

Cinobufocini inhibits NF-κB and COX-2 activation induced by TNF-α in lung adenocarcinoma cells

et al. 2012

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Abstract. The aim of the present study was to investigate the effects of cinobufocini on nuclear factor-κB (NF-κB), cyclooxygenase-2 (COX-2) and the production of cytokines induced by tumor necrosis factor-α (TNF-α) in the A549 cell line. A549 cells were incubated with cinobufocini at different concentrations for 24, 48 or 72 h. Cell proliferation was examined by the WST-8 assay. The expression of NF-κB, COX-2 and inhibitor κBα (IκBα) was studied by western blotting. The NF-κB-dependent luciferase rporter (3xκB-luc) was transfected for 24 h, the cells were treated with the reagents for 24 h, and the transcriptional activity of the NF-κB promoter was detected by a luciferase assay. The levels of IL-6 and IL-8 mRNA were detected by reverse transcription-polymerase chain reaction. We found that cinobufocini inhibited NF-κB p65 expression and the transcriptional activity of the NF-κB promoter induced by TNF-α compared with the control in the nuclei of A549 cells. Moreover, induced COX-2 expression was blocked by cinobufocini and was correlated with a reduction in the activated p65 subunit of NF-κB. Additionally, the levels of IL-6 and IL-8 mRNA induced by TNF-α were significantly suppressed by the addition of cinobufocini. In conclusion, these results suggest that the anti-inflammatory effects of cinobufocini are dependent on the NF-κB/COX-2 pathway in A549 cells, thereby providing a possible anticancer mechanism for the compound.

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“…Even though this concept implies the evolvement of novel tumor cell phenotypes by site-specific metastasis, the continual exchange of tumor cell phenotypes between the tumor cell colonies tends to equalize the molecular profiles of the primary tumor and its metastases [62,63]. Experimental evidence for the existence of tumor self-seeding was provided by mouse models, which also showed that the tumor-derived cytokines IL-6 and IL-8 act as CTC attractants and for example the actin cytoskeleton component fascin-1 mediates the CTC infiltration into the mammary tumors [64].…”

Section: Emergence Of Novel Phenotypesmentioning

confidence: 94%

The Interrelating Dynamics of Hypoxic Tumor Microenvironments and Cancer Cell Phenotypes in Cancer Metastasis

Bartkowiak

Pantel

2011

Cancer Microenvironment

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The interrelating dynamics of the primary tumor cells and their surrounding microenvironment might determine phenotypic characteristics of disseminated tumor cells and contribute to cancer metastasis. Cytoprotective mechanisms (e.g., energy metabolism control, DNA damage response, global translation control and unfolded protein response) exert selective pressure in the tumor microenvironment. In particular, adaptation to hypoxia is vital for survival of malignant cells in the tumor and at distant sites such as the bone marrow. In addition to the stress response, the ability of tumor cells to undergo certain cellular re-differentiation programmes like the epithelial-mesenchymal transition (EMT), which is linked to cancer stemness, appears to be important for successful cancer cell spread. Here we will discuss the selection pressures that eventually lead to the formation of overt metastases. We will focus the properties of the microenvironment including (i) metabolic and cytoprotective programs that ensure survival of disseminated tumor cells, (ii) blood vessel structure, and (iii) the hypoxianormoxia switch as well as intrinsic factors affecting the evolvement of novel tumor cell populations.

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Tumor Self-Seeding by Circulating Cancer Cells

Cited by 1,173 publications

References 47 publications

Chemokines in tumor development and progression

Chemokines in tumor development and progression

Cinobufocini inhibits NF-κB and COX-2 activation induced by TNF-α in lung adenocarcinoma cells

The Interrelating Dynamics of Hypoxic Tumor Microenvironments and Cancer Cell Phenotypes in Cancer Metastasis

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