Kaplan et al. reply

Kaplan, Rosandra N.; Riba, Rebecca D.; Zacharoulis, Stergios; Bramley, Anna H.; Vincent, Loı̈c; Costa, Carla; MacDonald, Daniel D.; Jin, David; Shido, Koji; Kerns, Scott; Zhu, Zhenping; Hicklin, Daniel J.; Wu, Yan; Port, Jeffrey L.; Altorki, Nasser K.; Port, Elisa; Ruggero, Davide; Shmelkov, Sergey V.; Jensen, Kristian K.; Rafii, Shahin; Lyden, David; Wels, Jared

doi:10.1038/nature08261

Cited by 46 publications

(73 citation statements)

References 15 publications

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“…MMP-9 is known to contribute to the malignant behavior of tumor cells through multiple mechanisms of action [6][7][8]. The invasion assay utilizing Matrigel-coated membranes is routinely used as a means of assessing cell invasiveness, which correlates with metastatic potential [17][18][19].…”

Section: Discussionmentioning

confidence: 99%

“…Recent work on metastasis has led to the new concept that under the direction of tumor cells, normal host cells select a microenvironment suitable for metastasis [6]. The notion that MMPs are essential for the infiltration of tumor cells into surrounding tissue is important, particularly since malignant tumors continue to be leading GD1a NEGATIVELY REGULATES MMP-9 EXPRESSION 199 causes of death in developed countries.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Ganglioside GD1a Negatively Regulates Matrix Metalloproteinase-9 Expression in Mouse FBJ Cell Lines at the Transcriptional Level

Huang

Man

Wang

et al. 2007

Connective Tissue Research

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Mouse FBJ virus-induced osteosarcoma FBJ-S1 cells rich in GD1a are not readily metastatic, whereas FBJ-LL cells with low levels of GD1a are highly metastatic. GD1a was previously shown to suppress metastasis of mouse FBJ cells and to upregulate caveolin-1 and stromal interaction molecule 1 expression. The present study demonstrates that matrix metalloproteinase-9 (MMP-9) expression renders FBJ-LL cells invasive. MMP-9 is inversely regulated by GD1a, based upon four observations: MMP-9 mRNA content was 5 times higher in FBJ-LL cells than FBJ-S1 cells; a GD1a-re-expressing FBJ-LL cell variant produced through beta1,4GalNAcT-1 cDNA transfection expressed lower levels of MMP-9; exogenous addition of GD1a to FBJ-LL cells decreased MMP-9 production in a dose- and time-dependent manner; and treatment of GD1a-rich cells with D-PDMP or siRNA targeting St3gal2 decreased GD1a expression, but augmented MMP-9 expression. This is the first report demonstrating that GD1a negatively regulates expression of MMP-9 at the transcriptional level.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Ganglioside GD1a Negatively Regulates Matrix Metalloproteinase-9 Expression in Mouse FBJ Cell Lines at the Transcriptional Level

Huang

Man

Wang

et al. 2007

Connective Tissue Research

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“…In fact, an active contribution of the stroma to growth and invasion of malignant tumors [100,[175][176][177][178] likely is supported by carcinomaassociated fibroblasts, that are a major source of CXCL12 [178]. Tumor-associated fibroblasts secrete CXCL12 [179], that attracts CXCR4 expressing tumor cells as well as endothelial cell progenitors, thus promoting angiogenesis [180]. It is suggested that the CXCL12 -CXCR4 axis plays a pivotal role in directing metastasis of CXCR4 + tumor cells towards organs with high CXCL12 expression, like lymph nodes, lung, liver and bones.…”

Section: Stem Cell Homing and The Pre-metastatic Nichementioning

confidence: 98%

“…Of particular interest with respect to HSC / CIC migration is the study of Kaplan et al [179], that describes the formation of a pre-metastatic niche. Using mouse models, the authors noted that in the organs where tumor cells are likely to settle and grow, niches can be detected that later on will house the metastatic cells.…”

Section: Stem Cell Homing and The Pre-metastatic Nichementioning

confidence: 99%

CD44 and EpCAM: Cancer-Initiating Cell Markers

Marhaba

Klingbeil²,

Nuebel³

et al. 2008

CMM

169

130

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Embryonic stem cells are immortal, can self renew, and differentiate into all cells of the body. The adult organism maintains adult stem cells in regenerative organs that can differentiate into all cells of the respective organ. Virchow's hypothesis that cancer may arise from embryonic-like cells has received strong support, as it was demonstrated that tumors contain few cells, known as cancer stem or cancer-initiating cells (CIC), that account for primary and metastatic tumor growth. CIC are mostly defined by expression of CIC-markers that are associated and correlated with the potential of CIC to grow in xenogeneic mice. CIC marker profiles have been elaborated for many tumors, with several markers as CD24, CD44, CD133, CD166, EpCAM, and some integrins, being expressed by tumors of different histological type. Their function in promoting CIC maintenance and activity is largely unknown. The fate of stem cells, determined by their position, is minutely regulated by few adjacent cells creating a niche. CIC also require a niche, mostly for settlement and growth in distant organs. This so called pre-metastatic niche is initiated by the primary tumor before metastasizing cell arrival. How do CIC prepare the pre-metastatic niche? Cancer cells secrete a matrix that serves a cross-talk with surrounding tissues. Additionally, cancer cells can abundantly deliver exosomes, which function as long-distance intercellular communicators. Studies on a rat pancreatic adenocarcinoma support our hypothesis that tumor-derived matrix and exosomes are the main actors in forming the pre-metastatic niche with CIC markers being engaged in matrix preparation and/or exosome delivery.

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“…Together, all these facilitate tumor growth, progression and spread. 30,42,44 However, the effects of migratory potential of cells on their proliferative and metastasizing behavior would be difficult to isolate or single out in such a complex system. Thus, it is in this context that 2D migration analyses become useful.…”

Section: Introductionmentioning

confidence: 99%

Collective Migration Behaviors of Human Breast Cancer Cells in 2D

Mendoz

Lim

2011

Cel. Mol. Bioeng.

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Cancer related deaths are mainly attributed to the spread of cancer cells to distant organs to form secondary tumors by a process called metastasis. Migration is one of the factors among many others that are strongly implicated in this phenomenon. Here we studied the migratory behavior of benign (MCF-10A), non-invasive malignant (MCF-7) and highly-invasive malignant (MDA-MB-231) tumor cell lines which are derivatives of ductal epithelium of the human breast, using a modified ring cell migration assay technique. Time lapse phase contrast video microscopy was used to monitor migration on both culture coated and Collagen-IV coated surfaces. Individual cells were tracked for 24 h and observations were made on the morphological development of the lamellipods. Analyses show that an intact intercellular adhesion coupled with unidirectional lamellipod formation in benign cells help to coordinate migratory behavior when compared against the malignant variants. Among the cancer cell lines, the non-invasive malignant cells had shorter migratory distances and exhibited pseudo-coordinated behavior due to altered or defective lamellipod morphology and intercellular adhesion, while the highly invasive malignant cells displayed individualistic and chaotic movements with little or no intercellular adhesion. Collagen-IV coating increased the migration rates of the highly invasive cell lines, while the effect was less pronounced on the other two cell lines.

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Kaplan et al. reply

Cited by 46 publications

References 15 publications

Ganglioside GD1a Negatively Regulates Matrix Metalloproteinase-9 Expression in Mouse FBJ Cell Lines at the Transcriptional Level

Ganglioside GD1a Negatively Regulates Matrix Metalloproteinase-9 Expression in Mouse FBJ Cell Lines at the Transcriptional Level

CD44 and EpCAM: Cancer-Initiating Cell Markers

Collective Migration Behaviors of Human Breast Cancer Cells in 2D

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