HGF and ligation of αvβ5 integrin induce a novel, cancer cell-specific gene expression required for cell scattering

Crouch, Sonya; Spidel, Celee S; Lindsey, J. Suzanne

doi:10.1016/j.yexcr.2003.09.016

Cited by 33 publications

(93 citation statements)

References 60 publications

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“…6 Endogenous Mig-7 expression was reduced with siRNA. In brief, three Mig-7-spe-cific siRNAs sequences (Table 1) were designed by Ambion (Austin, TX) with BamHI and HindIII restriction enzyme sites at each 5Ј and 3Ј, respectively, for directional cloning.…”

Section: Expression Of Mig-7 Flag-tagged Protein and Mig-7-specific Smentioning

confidence: 99%

“…26 HEC1A, RL95-2 (RL95) endometrial carcinoma, and HT29 colon carcinoma cell lines (all from American Type Culture Collection, Rockville, MD) were cultured as described previously. 6,23 Epidermal growth factor (EGF; Calbiochem, La Jolla, CA) or HGF/SF (R&D Systems, Minneapolis, MN) treatments (each at 20 ng/ml) were incubated for the indicated time with RL95 cells that had been serum-starved for 12 hours. Melanoma cell lines, MUM-2B, MUM-2C, C918, C8161, and A375P, were maintained in RPMI 1640 medium (Life Technologies, Inc., Invitrogen, Grand Island, NY) supplemented with 10% fetal bovine serum (Life Technologies, Inc., Invitrogen), 20 mmol/L HEPES, and 0.1% gentamicin sulfate.…”

Section: Cell Culturesmentioning

confidence: 99%

“…4 Invasion of these two cell types is initiated by receptor tyrosine kinase (RTK) and ␣v␤5 signaling cross talk. [5][6][7][8] Data suggest that highly invasive cancer cells can form conduits in tumors, a process some researchers call vasculogenic mimicry. 9 -11 Previous publications have described tumor cells lining the lumen of irregular and leaky tumor vessels (see review 12 ).…”

mentioning

confidence: 99%

“…Notably, Mig-7 is not detected in 25 different normal human tissues or in blood from normal patients. 6,23 Signaling that initiates CTBs and tumor cell invasion from RTK c-Met, the hepatocyte growth factor/ scatter factor (HGF/SF) receptor, and ␣v␤5 integrin induces Mig-7 expression. 6,8,24 Based on these data, we hypothesized that Mig-7 expression plays a role in behaviors in common between CTBs and carcinoma cells, namely invasion and vascular cell mimicry.…”

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confidence: 99%

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Overexpression of Carcinoma and Embryonic Cytotrophoblast Cell-Specific Mig-7 Induces Invasion and Vessel-Like Structure Formation

Petty

Garman

Winn

et al. 2007

The American Journal of Pathology

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Molecular requirements for carcinoma cell interactions with the microenvironment are critical for disease progression but are poorly understood. Integrin ␣v␤5, which senses the extracellular matrix, is important for carcinoma cell dissemination in vivo. ␣v␤5 signaling induces Mig-7, a novel human gene product that is apparently carcinoma-specific. We hypothesized that Mig-7 expression facilitates tumor cell dissemination by increasing invasion and vasculogenic mimicry. Results show that embryonic cytotrophoblasts up-regulated Mig-7 expression before they acquired an invasive phenotype capable of pseudovasculogenesis. Mig-7 protein primarily co-localized with vasculogenic mimicry markers factor VIII-associated antigen, vascular endothelial-cadherin, and laminin 5 ␥2 chain domain III fragment in lymph node metastases. Overexpression of Mig-7 increased ␥2 chain domain III fragments known to contain epidermal growth factor (EGF)-like repeats that can activate EGF receptor. Interestingly, EGF also induced Mig-7 expression. Carcinoma cell adhesion to laminins was significantly reduced by Mig-7 expression. Remarkably, in two-dimensional and three-dimensional Matrigel cultures, Mig-7 expression caused invasion and vessel-like structures. Melanoma cells, which were previously characterized to invade aggressively and to undergo vasculogenic mimicry, expressed Mig-7. Taken together, these data suggest that Mig-7 expression allows cells to sense their environment, to invade, and to form vessel-like structures through a novel relationship with laminin 5 ␥2 chain domain III fragments.

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Section: Expression Of Mig-7 Flag-tagged Protein and Mig-7-specific Smentioning

confidence: 99%

Section: Cell Culturesmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Overexpression of Carcinoma and Embryonic Cytotrophoblast Cell-Specific Mig-7 Induces Invasion and Vessel-Like Structure Formation

Petty

Garman

Winn

et al. 2007

The American Journal of Pathology

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“…First described by Crouch et al in 2004, who studied MIG-7 protein with an antibody to its first nine amino acids and demonstrated reproducible and significant inhibition of endometrial carcinoma cell invasion in vitro [15]. MIG-7 protein has been proposed as one of the essential factors that facilitate tumor cell dissemination by aggregate invasion and by promoting the process of vasculogenic mimicry [15].…”

Section: Introductionmentioning

confidence: 99%

Mig-7 expression and vasculogenic mimicry in malignant ovarian tumors

Czekierdowski

Czekierdowska

Stachowicz³

et al. 2017

Ginekol Pol

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Objectives:To investigate the possible association of vasculogenic mimicry (VM), VE-cadherin and MIG-7 expression with clinicopathological features of women with malignant ovarian masses. Material and methods:VM was studied with the PAS reaction and VE-cadherin was assessed with immunohistochemistry in 108 women with malignant ovarian tumors. Additionally, quantitative expression of MIG-7 mRNA was performed in 52 ovarian cancers with qRT-PCR.Results: VM was found in 48/108 cases (44%), more often in higher FIGO stage tumors (83% cases; 40 vs. 8; p = 0.01). High expression of VE-cadherin was present in 37% of all ovarian masses. Ovarian tumors without VM more often expressed low levels of VE-cadherin than tumors where VM was found (37.6% vs.14.6%). No expression or very low expression of MIG-7 mRNA was found in all normal ovarian tissues and in 32 cancer samples. Median RQ of MIG-7 mRNA in tumor samples was higher than in normal ovarian tissue (RQ = 0.29 vs. RQ = 0.05, respectively; p < 0.005) and higher than in non-malignant ovarian masses (0.98 vs. 0.05 respectively; p = 0.03). Expression of MIG-7 mRNA was significantly correlated with VM (p = 0.039). In tumors with PAS-positive structures median RQ MIG-7 mRNA was higher than in tumors with PAS-negative findings (1.89 vs. 0.13 respectively). VE-cadherin expression was more frequently found in tumors where MIG-7 mRNA was present (p = 0.004). Conclusions:Vasculogenic mimicry exists in malignant ovarian tumors and advanced clinical stages of malignancy are accompanied by a high incidence of VM formation. MIG-7 mRNA and VE-cadherin expression may serve as additional molecular markers of VM in ovarian malignancies.

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Hepatocyte growth factor differently influences Met-E-cadherin phosphorylation and downstream signaling pathway in two models of breast cells

Matteucci

Ridolfi

Desiderio

2006

Cell. Mol. Life Sci.

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E-cadherins are implicated in cell adhesion, and also in cell signaling by associating with tyrosine kinase-receptors such as Met, the hepatocyte growth factor (HGF) receptor. Using two different cellular models, i.e. MCF-7 (breast carcinoma) and MCF-10 (immortalized mammary) cells, we studied the possible mechanism(s) by which E-cadherins modulate the signaling pathways downstream of Met, leading to beta-catenin-TCF transcriptional activity. In MCF-7, but not in MCF-10 cells, E-cadherins were remarkably associated with Met. Moreover, in MCF-7 cells both co-immunoprecipitation with anti-Met antibody and co-localization were increased by 30-min HGF treatment, which caused E-cadherin tyrosine phosphorylation. Also beta-catenin in the co-immunoprecipitate was phosphorylated by HGF, probably favoring TCF activation. Consistently, after HGF treatment, beta-catenin redistributed earlier in MCF-7 than in MCF-10 cells, with nuclear accumulation and activation of TOPFLASH gene reporter. Our results indicate a functional role of Met-E-cadherin interaction in MCF-7 cells through the amplification of the signaling downstream of HGF-Met triggering that involved c-Src and phosphoinositide-3-kinase activities.

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HGF and ligation of αvβ5 integrin induce a novel, cancer cell-specific gene expression required for cell scattering

Cited by 33 publications

References 60 publications

Overexpression of Carcinoma and Embryonic Cytotrophoblast Cell-Specific Mig-7 Induces Invasion and Vessel-Like Structure Formation

Overexpression of Carcinoma and Embryonic Cytotrophoblast Cell-Specific Mig-7 Induces Invasion and Vessel-Like Structure Formation

Mig-7 expression and vasculogenic mimicry in malignant ovarian tumors

Hepatocyte growth factor differently influences Met-E-cadherin phosphorylation and downstream signaling pathway in two models of breast cells

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