Inducible expression of tissue factor in small-cell lung cancer: impact on morphology and matrix metalloproteinase secretion

Hahn, Nicole; Heiden, M.; Seitz, Rainer; Salge-Bartels, Ursula

doi:10.1007/s00432-011-1139-1

Cited by 10 publications

(5 citation statements)

References 24 publications

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“…In preliminary studies, we were unable to detect FX mRNA expression in melanoma cells by RT-PCR. However, FX is frequently detected in several cancer specimens, including melanoma (18), and may be locally delivered to the tumor microenvironment by macrophages/inflammatory cells that bind FX through Mac-1 (43). These observations together with the fact that hypoxia in multiple cancers also enhances expression of FVII (44), lend further support for a critical role of MDA-9/syntenin in the TF⅐FVIIa⅐Xa/PAR-1 signaling axis that regulates cell motility and tumor progression.…”

Section: Discussionmentioning

confidence: 99%

MDA-9/Syntenin Is Essential for Factor VIIa-induced Signaling, Migration, and Metastasis in Melanoma Cells

Aissaoui

Prévost

Boucharaba

et al. 2015

Journal of Biological Chemistry

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Background: MDA-9/syntenin and tissue factor (TF) are overexpressed in most types of human cancer. Results: Induction of MDA-9/syntenin in melanoma involves the binding of FVIIa and FX to TF on the cell surface, which initiates a signaling circuit essential for cell motility and metastasis of melanoma. Conclusion: MDA-9/syntenin is an important TF-regulated gene. Significance: Targeting TF-mediated MDA-9/syntenin may represent a novel therapeutic strategy for eliminating cancer.

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Section: Discussionmentioning

confidence: 99%

MDA-9/Syntenin Is Essential for Factor VIIa-induced Signaling, Migration, and Metastasis in Melanoma Cells

Aissaoui

Prévost

Boucharaba

et al. 2015

Journal of Biological Chemistry

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“…Our findings align with the induction of proangiogenic activities by microvesicles shed by cancer cells through a CD147-mediated mechanism [47]. Evidence also suggests that TF-mediated signaling in cancer cells plays a role in promoting invasion by upregulating the expression of MMPs [48].…”

Section: Discussionsupporting

confidence: 85%

Targeting cancer-derived extracellular vesicles by combining CD147 inhibition with tissue factor pathway inhibitor for the management of urothelial cancer cells

Boddu,

Zamzow,

Kramer

et al. 2024

Cell Commun Signal

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Background Extracellular vesicles (EVs), including microvesicles, hold promise for the management of bladder urothelial carcinoma (BLCA), particularly because of their utility in identifying therapeutic targets and their diagnostic potential using easily accessible urine samples. Among the transmembrane glycoproteins highly enriched in cancer-derived EVs, tissue factor (TF) and CD147 have been implicated in promoting tumor progression. In this in vitro study, we explored a novel approach to impede cancer cell migration and metastasis by simultaneously targeting these molecules on urothelial cancer-derived EVs. Methods Cell culture supernatants from invasive and non-invasive bladder cancer cell lines and urine samples from patients with BLCA were collected. Large, microvesicle-like EVs were isolated using sequential centrifugation and characterized by electron microscopy, nanoparticle tracking analysis, and flow cytometry. The impact of urinary or cell supernatant-derived EVs on cellular phenotypes was evaluated using cell-based assays following combined treatment with a specific CD147 inhibitor alone or in combination with a tissue factor pathway inhibitor (TFPI), an endogenous anticoagulant protein that can be released by low-molecular-weight heparins. Results We observed that EVs obtained from the urine samples of patients with muscle-invasive BLCA and from the aggressive bladder cancer cell line J82 exhibited higher TF activity and CD147 expression levels than did their non-invasive counterparts. The shedding of GFP-tagged CD147 into isolated vesicles demonstrated that the vesicles originated from plasma cell membranes. EVs originating from invasive cancer cells were found to trigger migration, secretion of matrix metalloproteinases (MMPs), and invasion. The same induction of MMP activity was replicated using EVs obtained from urine samples of patients with invasive BLCA. EVs derived from cancer cell clones overexpressing TF and CD147 were produced in higher quantities and exhibited a higher invasive potential than those from control cancer cells. TFPI interfered with the effect when used in conjunction with the CD147 inhibitor, further suppressing homotypic EV-induced migration, MMP production, and invasion. Conclusions Our findings suggest that combining a CD147 inhibitor with low molecular weight heparins to induce TFPI release may be a promising therapeutic approach for urothelial cancer management. This combination can potentially suppress the tumor-promoting actions of cancer-derived microvesicle-like EVs, including collective matrix invasion. Graphical Abstract

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“…MMPs can promote cancer progression by increasing cancer-cell growth,migration, invasion, metastasis and angiogenesis, and their expression is often associated with poor survival (Cao et al, 2011;Im et al, 2012). MMP-2 is considered to play a critical role in metastasis, and the synthesis and secretion of MMP-2 can be stimulated by a variety of stimuli, including cytokines, during various pathological processes such as tumor invasion, atherosclerosis, and inflammation (Cao et al, 2011;Hahn et al, 2012). MMP-1 2 C735T and C1306T are two common polymorphisms in the MMP-2 gene, have allele-specific effects on the transcriptional activities of MMP gene promoters (Decock et al, 2008;Chetty et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Quantitative Assessment of the Effects of MMP-2 Polymorphisms on Lung Carcinoma Risk

Guo

Wang²,

Zhang³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Background: Previous studies assessing associations between matrix metalloproteinase 2 (MMP-2) polymorphisms and lung cancer risk reported conflicting results. A meta-analysis was therefore performed to derive a more precise estimation. Method: Case-control studies assessing associations between MMP-2 C735T and C1306T polymorphisms and lung cancer risk were included. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were estimated. Results: 7 studies with a total of 3,189 lung cancer cases and 3,013 controls were finally included into this meta-analysis. Overall, the MMP-2 C735T polymorphism was associated with lung cancer risk under the homozygote model (CC versus TT: OR =1.44, 95% CI = 1.03-2.02, I 2 = 0%), while the MMP-2 C1306T polymorphism also associated demonstrated links with all four models (all P values less than 0.05). Subgroup analyses by race suggested obvious associations between MMP-2 C735T and C1306T polymorphisms and lung cancer risk in Asians but not in Caucasians. There was no evidence for publication bias. Conclusion: Currently available evidence supports teh conclusion that MMP-2 C735T and C1306T polymorphisms influence susceptibility to lung cancer in Asians.

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Inducible expression of tissue factor in small-cell lung cancer: impact on morphology and matrix metalloproteinase secretion

Cited by 10 publications

References 24 publications

MDA-9/Syntenin Is Essential for Factor VIIa-induced Signaling, Migration, and Metastasis in Melanoma Cells

MDA-9/Syntenin Is Essential for Factor VIIa-induced Signaling, Migration, and Metastasis in Melanoma Cells

Targeting cancer-derived extracellular vesicles by combining CD147 inhibition with tissue factor pathway inhibitor for the management of urothelial cancer cells

Quantitative Assessment of the Effects of MMP-2 Polymorphisms on Lung Carcinoma Risk

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