Procoagulant (Tissue Factor) Activity Is Higher In Cells From Murine Sarcoma Sublines With Lower Metastatic Potential

1981 ◽  
Author(s):  
M Colucci ◽  
R Giavazzi ◽  
G Alessandri ◽  
N Semeraro ◽  
A Mantovani ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cancer Cell ◽  
Metastatic Potential ◽  
Procoagulant Activity ◽  
Autologous Plasma ◽  
Parent Line ◽  
Metastatic Capacity ◽  
Cell Invasiveness

It has been suggested that cancer cell procoagulant activity influences metastasis formation by promoting fibrin deposition around tumors. We have investigated the procoagulant activity of various tumor cell sublines with different metastatic capacity. These were derived from spontaneous lung nodules of mFS6, a benzopyrene-induced sarcoma in C57B1/6 mice. After one in vivo passage by s.c. implantation, the resulting tumor was cultured once in vitro till confluence; cells were then harvested from plastic bottles by trypsin treatment, and washed extensively after trypsin neutralization. Tumor cell procoagulant activity was measured by a one-stage clotting assay using autologous plasma. All the cells tested possessed thromboplastin-like activity since they shortened the recalcification time of normal and factor VUI-deficient plasma to a similar extent but had no activity on factor Vll-deficient plasma.They were, however, heterogeneous as regards the degree of procoagulant activity; the two cell lines with virtually no metastatic capacity showed 6-8 times higher procoagulant activity than the cells from the parent line; in contrast, the procoagulant activity of the two sublines with higher metastatic capacity did not differ significantly from that of the parent line.These findings support the hypothesis that fibrin is part of a defence reaction against cancer cell invasiveness.

scholarly journals Procoagulant activity of sarcoma sublines with different metastatic potential

Blood ◽  
1981 ◽  
Vol 57 (4) ◽  
pp. 733-735 ◽  
Author(s):  
M Colucci ◽  
R Giavazzi ◽  
G Alessandri ◽  
N Semeraro ◽  
A Mantovani ◽  
...  
Keyword(s):  
Cancer Cell ◽  
Metastatic Potential ◽  
Procoagulant Activity ◽  
Fibrin Deposition ◽  
Defence Reaction ◽  
Parent Line ◽  
Metastatic Capacity ◽  
Murine Fibrosarcoma ◽  
Cell Invasiveness ◽  
Cancer Cell Invasiveness

Abstract It has been suggested that cancer cell procoagulant activity influences metastasis formation by promoting fibrin deposition around tumors. We have investigated the procoagulant activity of various tumor cell sublines with different metastatic capacity derived from metastatic nodules of a murine fibrosarcoma. All the cells tested possessed a marked thromboplastin-like activity; they were, however, heterogeneous as regards the degree of procoagulant activity; the two cell lines with virtually no metastatic capacity showed 6--8 times higher procoagulant activity than the cells from the parent line; in contrast, the procoagulant activity of the two sublines with higher metastatic capacity did not differ significantly from that of the parent line. These findings support the hypothesis that fibrin is part of a defence reaction against cancer cell invasiveness.

scholarly journals Procoagulant activity of sarcoma sublines with different metastatic potential

Blood ◽  
1981 ◽  
Vol 57 (4) ◽  
pp. 733-735
Author(s):  
M Colucci ◽  
R Giavazzi ◽  
G Alessandri ◽  
N Semeraro ◽  
A Mantovani ◽  
...  
Keyword(s):  
Cancer Cell ◽  
Metastatic Potential ◽  
Procoagulant Activity ◽  
Fibrin Deposition ◽  
Defence Reaction ◽  
Parent Line ◽  
Metastatic Capacity ◽  
Murine Fibrosarcoma ◽  
Cell Invasiveness ◽  
Cancer Cell Invasiveness

It has been suggested that cancer cell procoagulant activity influences metastasis formation by promoting fibrin deposition around tumors. We have investigated the procoagulant activity of various tumor cell sublines with different metastatic capacity derived from metastatic nodules of a murine fibrosarcoma. All the cells tested possessed a marked thromboplastin-like activity; they were, however, heterogeneous as regards the degree of procoagulant activity; the two cell lines with virtually no metastatic capacity showed 6--8 times higher procoagulant activity than the cells from the parent line; in contrast, the procoagulant activity of the two sublines with higher metastatic capacity did not differ significantly from that of the parent line. These findings support the hypothesis that fibrin is part of a defence reaction against cancer cell invasiveness.

scholarly journals Metastatic potential severely altered by changes in tumor cell adhesiveness and cell-surface sialylation.

1983 ◽  
Vol 157 (1) ◽  
pp. 371-376 ◽  
Author(s):  
M Fogel ◽  
P Altevogt ◽  
V Schirrmacher
Keyword(s):  
Sialic Acid ◽  
Cell Surface ◽  
Tumor Cell ◽  
Metastatic Potential ◽  
Lectin Receptors ◽  
Lectin Receptor ◽  
Receptor Sites ◽  
Variant Line

A plastic adherent variant line (ESb-M) of a highly invasive and metastatic murine T cell lymphoma (ESb) was found to have lost its metastatic potential while still being tumorigenic in normal syngeneic hosts. The variant retained most of its ESb-derived antigenic and biochemical characteristics but differed at binding sites for certain lectins with specificity for terminal N-acetylgalactosamine residues. Whereas such sites were masked by sialic acid on metastatic ESb cells, they became unmasked on the adherent variant line. Metastatic revertants of ESb-M cells did not express the respective lectin receptor sites because these were again masked by sialic acid. It is suggested that the masking of specific lectin receptors sites on the tumor cell surface is of crucial importance for metastatis. If freely exposed, these sites may change adherence characteristics of the cells possibly not only in vitro (to plastic) but also in vivo.

scholarly journals Cathepsin E enhances anticancer activity of doxorubicin on human prostate cancer cells showing resistance to TRAIL-mediated apoptosis

2010 ◽  
Vol 391 (8) ◽  
Author(s):  
Atsushi Yasukochi ◽  
Tomoyo Kawakubo ◽  
Seiji Nakamura ◽  
Kenji Yamamoto
Keyword(s):  
Prostate Cancer ◽  
Tumor Cell ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Down Regulation ◽  
Cathepsin E

Abstract We previously described that cathepsin E specifically induces growth arrest and apoptosis in several human prostate cancer cell lines in vitro by catalyzing the proteolytic release of soluble tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) from the tumor cell surface. It also prevents tumor growth and metastasis in vivo through multiple mechanisms, including induction of apoptosis, angiogenesis inhibition and enhanced immune responses. Using the prostate cancer cell line PPC-1, which is relatively resistant to cell death by doxorubicin (40–50% cytotoxicity), we first report that a combination treatment with cathepsin E can overcome resistance of the cells to this agent. In vitro studies showed that combined treatment of PPC-1 cells with the two agents synergistically induces viability loss, mainly owing to down-regulation of a short form of the FLICE inhibitory protein FLIP. The enhanced antitumor activity was corroborated by in vivo studies with athymic mice bearing PPC-1 xenografts. Intratumoral application of cathepsin E in doxorubicin-treated mice results in tumor cell apoptosis and tumor regression in xenografts by enhanced TRAIL-induced apoptosis through doxorubicin-induced c-FLIP down-regulation and by a decrease in tumor cell proliferation. These results indicate that combination of cathepsin E and doxorubicin is sufficient to overcome resistance to TRAIL-mediated apoptosis in chemoresistant prostate cancer PPC-1 cells, thus indicating therapeutic potential for clinical use.

scholarly journals Printing the Pathway Forward in Bone Metastatic Cancer Research: Applications of 3D Engineered Models and Bioprinted Scaffolds to Recapitulate the Bone–Tumor Niche

Cancers ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 507
Author(s):  
Anne M. Hughes ◽  
Alexus D. Kolb ◽  
Alison B. Shupp ◽  
Kristy M. Shine ◽  
Karen M. Bussard
Keyword(s):  
Cancer Research ◽  
Tumor Cell ◽  
Cancer Cell ◽  
Bone Tumor ◽  
Metastatic Cancer ◽  
Critical Role ◽  
Three Dimensional ◽  
Biocompatible Materials

Breast cancer commonly metastasizes to bone, resulting in osteolytic lesions and poor patient quality of life. The bone extracellular matrix (ECM) plays a critical role in cancer cell metastasis by means of the physical and biochemical cues it provides to support cellular crosstalk. Current two-dimensional in-vitro models lack the spatial and biochemical complexities of the native ECM and do not fully recapitulate crosstalk that occurs between the tumor and endogenous stromal cells. Engineered models such as bone-on-a-chip, extramedullary bone, and bioreactors are presently used to model cellular crosstalk and bone–tumor cell interactions, but fall short of providing a bone-biomimetic microenvironment. Three-dimensional bioprinting allows for the deposition of biocompatible materials and living cells in complex architectures, as well as provides a means to better replicate biological tissue niches in-vitro. In cancer research specifically, 3D constructs have been instrumental in seminal work modeling cancer cell dissemination to bone and bone–tumor cell crosstalk in the skeleton. Furthermore, the use of biocompatible materials, such as hydroxyapatite, allows for printing of bone-like microenvironments with the ability to be implanted and studied in in-vivo animal models. Moreover, the use of bioprinted models could drive the development of novel cancer therapies and drug delivery vehicles.

scholarly journals α2,3-Sialyltransferase ST3Gal III Modulates Pancreatic Cancer Cell Motility and Adhesion In Vitro and Enhances Its Metastatic Potential In Vivo

PLoS ONE ◽  
2010 ◽  
Vol 5 (9) ◽  
pp. e12524 ◽  
Author(s):  
Marta Pérez-Garay ◽  
Beatriz Arteta ◽  
Lluís Pagès ◽  
Rafael de Llorens ◽  
Carme de Bolòs ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Motility ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Metastatic Potential ◽  
Cancer Cell Motility ◽  
St3gal Iii

scholarly journals Inhibition of the Axl pathway impairs breast and prostate cancer metastasis to the bones and bone remodeling

2021 ◽  
Author(s):  
Mai Tanaka ◽  
Samantha S. Dykes ◽  
Dietmar W. Siemann
Keyword(s):  
Breast Cancer ◽  
Cell Signaling ◽  
Cancer Cell ◽  
Cancer Metastasis ◽  
Metastatic Potential ◽  
Breast Cancers ◽  
Neoplastic Cells ◽  
Breast And Prostate Cancer

AbstractApproximately 90% of cancer-related deaths result from cancer metastasis. In prostate and breast cancers, bone is the most common site of cancer cell dissemination. Key steps in the metastatic cascade are promoted through upregulation of critical cell signaling pathways in neoplastic cells. The present study assessed the role of the receptor tyrosine kinase Axl in prostate and breast cancer cell metastasis to bones using (i) Axl knockdown neoplastic cells and osteoclast progenitor cells in vitro, (ii) intracardiac injection of Axl knockdown tumor cells in vivo, and (iii) selective Axl inhibitor BGB324. Axl inhibition in neoplastic cells significantly decreased their metastatic potential, and suppression of Axl signaling in osteoclast precursor cells also reduced the formation of mature osteoclasts. In vivo, Axl knockdown in prostate and breast cancer cells significantly suppressed the formation and progression of bone metastases. Hence, therapeutic targeting of Axl may impair tumor metastasis to the bones through neoplastic and host cell signaling axes.

GENERATION OF ADP BY HUMAN AND MURINE TUMOR CELLS IS SPECIFIC BUT IS UNRELATED TO METASTATIC POTENTIAL

1987 ◽  
Author(s):  
G A Jamieson ◽  
G Grignani
Keyword(s):  
Tumor Cell ◽  
Metabolic Control ◽  
Tumor Cells ◽  
Cell Damage ◽  
Metastatic Potential ◽  
Iodoacetic Acid ◽  
Human Platelets ◽  
Significant Difference

The ability of tumor cells to activate platelets may facilitate the metastatic process. It has been generally assumed that the production of ADP by tumor cells is due to non-specific damage during harvesting in vitro or, in vivo, by frictional interactions with the capillary wall. The present work shows that tumor cell ADP arises not from cell damage but by a specific process under metabolic control. The human 253J urinary carcinoma cell line activated heparinized human platelets by an ADP-dependent mechanism based on inhibition by CP/CPK and the identification of aggregating concentrations (1 uM) of ADP in the cell-free supernatant by HPLC. Tumor cell damage during harvesting was shown not to be a factor since (i) the amount of ADP secreted was unrelated to the appearance of LDH, (ii) was similar when measured in confluent monolayers, in tumor cells after detachment and resuspension or following crossover studied in HBSS and MEM, and (iii) was constant at varying tumor cell concentrations. Metabolic control of ADP generation or transport was indicated by the fact that it was reduced 50 in tumor cells treated with p-chloromercuribenzene sulfonate and was completely abolished in those treated with iodoacetic acid. In order to determine whether this metabolically controlled generation of ADP was related to metastatic potential, we carried out identical experiments with the FI (low) and F10 (high) metastatic variants of the Bl6 murine melanoma line. The amounts of ADP produced by the B16 cells were about twice as great as with the human 253J cells but there was no significant difference between the amounts of ADP generated by FI and F10 variants. These studies demonstrate that ADP production by tumor cells is a discrete process under metabolic control but is not directly related to the metastatic potential of individual tumor cell lines.

Interaction between elastin and tumor cell lines with different metastatic potential; in vitro and in vivo studies

1991 ◽  
Vol 117 (3) ◽  
pp. 232-238 ◽  
Author(s):  
J. Timar ◽  
K. Lapis ◽  
T. Fulop ◽  
Z. S. Varga ◽  
J. M. Tixier ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Lines ◽  
Metastatic Potential ◽  
In Vivo Studies ◽  
Tumor Cell Lines

scholarly journals Hic-5 expression is a major indicator of cancer cell morphology, migration, and plasticity in three-dimensional matrices

2018 ◽  
Vol 29 (14) ◽  
pp. 1704-1717 ◽  
Author(s):  
Anushree C. Gulvady ◽  
Fatemeh Dubois ◽  
Nicholas O. Deakin ◽  
Gregory J. Goreczny ◽  
Christopher E. Turner
Keyword(s):  
Tumor Cell ◽  
Cell Lines ◽  
Cancer Cell ◽  
Ectopic Expression ◽  
Three Dimensional ◽  
Cell Types ◽  
Cell Phenotype ◽  
In Vitro Invasiveness

The focal adhesion proteins Hic-5 and paxillin have been previously identified as key regulators of MDA-MB-231 breast cancer cell migration and morphologic mesenchymal-amoeboid plasticity in three-dimensional (3D) extracellular matrices (ECMs). However, their respective roles in other cancer cell types have not been evaluated. Herein, utilizing 3D cell–derived matrices and fibronectin-coated one-dimensional substrates, we show that across a variety of cancer cell lines, the level of Hic-5 expression serves as the major indicator of the cells primary morphology, plasticity, and in vitro invasiveness. Domain mapping studies reveal sites critical to the functions of both Hic-5 and paxillin in regulating phenotype, while ectopic expression of Hic-5 in cell lines with low endogenous levels of the protein is sufficient to induce a Rac1-dependent mesenchymal phenotype and, in turn, increase amoeboid-mesenchymal plasticity and invasion. We show that the activity of vinculin, when coupled to the expression of Hic-5 is required for the mesenchymal morphology in the 3D ECM. Taken together, our results identify Hic-5 as a critical modulator of tumor cell phenotype that could be utilized in predicting tumor cell migratory and invasive behavior in vivo.

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