scholarly journals Proteolytic Activity During the Growth of C6 Astrocytoma in the Murine Spheroid Implantation Model

1992 ◽  
Vol 19 (1) ◽  
pp. 17-22 ◽  
Author(s):  
Indrasen S. Vaithilingam ◽  
Warren McDonald ◽  
Eric C. Stroude ◽  
Robert A. Cook ◽  
Rolando F. Del Maestro
Keyword(s):  
Proteolytic Activity ◽  
Tumor Tissue ◽  
Maximal Activity ◽  
Vascular Basement Membrane ◽  
Astrocytoma Cells ◽  
Maximum Value ◽  
C6 Astrocytoma ◽  
Cerebral Cortex Tissue ◽  
Collagenase Iv ◽  
Implantation Model

ABSTRACT:General protease and collagenase IV activity are involved in the remodelling of the vascular basement membrane that occurs during tumor-induced angiogenesis. This study has assessed the level of these enzymes in tumor, peritumoral or contralateral cerebral cortex tissue during the growth of C6 astrocytoma in the rat spheroid implantation model. General proteolytic activity was increased in tumor tissue beginning on day 8 following spheroid implantation, then increased to a maximum value on day 11 and decreased to control values on day 18. A similar pattern was seen for collagenase IV activity but maximal activity occurred on day 13. The peritumor and tumor patterns of activity were similar. General protease activity was increased in the hemisphere contralateral to the tumor suggesting that the growth of C6 astrocytoma in rat brain was influencing biochemical events distant from the tumor. C6 astrocytoma cells orchestrate a cascade of proteolytic events which may play a crucial role in angiogenesis associated with tumor growth in the model system studied.

Serum proteolytic activity during the growth of C6 astrocytoma

1992 ◽  
Vol 77 (4) ◽  
pp. 595-600 ◽  
Author(s):  
Indrasen S. Vaithilingam ◽  
Warren McDonald ◽  
Noel K. Brown ◽  
Eric Stroude ◽  
Robert A. Cook ◽  
...  
Keyword(s):  
Proteolytic Activity ◽  
Type Iv Collagen ◽  
Collagenase Activity ◽  
Type Iv Collagenase ◽  
Content Type ◽  
Type Iv ◽  
Astrocytoma Cells ◽  
Vessel Remodeling ◽  
C6 Astrocytoma ◽  
Fine Print

✓ Tumor growth is dependent on the ability of neoplastic cells to induce angiogenesis. Blood-vessel remodeling requires the reconstruction of the nonfibrous proteins and type IV collagen components of the basement membrane. This study has assessed the influence of the growth of C6 astrocytoma cells in the rat spheroid implantation model on serum general protease and type IV collagenase activity. The results demonstrate that general protease activity increased in serum, reaching maximum values on Day 6 and Day 13 following spheroid implantation, and that type IV collagenase activity increased in serum, obtaining maximum values on Day 8 and Day 15. The measurement of serum proteolytic activity may be of value in the detection of recurrent tumors.

General protease and collagenase (IV) activity in C6 astrocytoma cells, C6 spheroids and implanted C6 spheroids

1991 ◽  
Vol 10 (3) ◽  
pp. 203-212 ◽  
Author(s):  
Indrasen S. Vaithilingam ◽  
Eric C. Stroude ◽  
Warren McDonald ◽  
Rolando F. Del Maestro
Keyword(s):  
Astrocytoma Cells ◽  
C6 Astrocytoma ◽  
Collagenase Iv

Release of collagen type IV degrading activity from C6 astrocytoma cells and cell density

1996 ◽  
Vol 84 (6) ◽  
pp. 1013-1019 ◽  
Author(s):  
Masashi Tamaki ◽  
Warren McDonald ◽  
Rolando F. Del Maestro
Keyword(s):  
Cell Density ◽  
Collagen Type ◽  
Cell Communication ◽  
Collagen Type Iv ◽  
Major Protein ◽  
Content Type ◽  
Type Iv ◽  
Astrocytoma Cells ◽  
C6 Astrocytoma

✓ Type IV collagen is a major protein component of the vascular basement membrane and its degradation is crucial to the initiation of tumor-associated angiogenesis. The authors have investigated the influence of cell density on the release of collagen type IV degrading activity by C6 astrocytoma cells in monolayer culture. The release of collagen type IV degrading activity was assessed biochemically, immunocytochemically, and by Western blot analysis. The results demonstrate that increasing plating density and increasing cell density are associated with decreased collagen type IV degrading activity released per tumor cell. These findings indicate the existence of regulatory mechanisms dependent on cell—cell communication, which modulate release of collagen type IV degrading activity. The extrapolation of these results to the in vivo tumor microenvironment would suggest that individual and/or small groups of invading tumor cells, distant from the main tumor mass, would release substantial collagen type IV degrading activity, which may be crucial to their continued invasion and to angiogenesis.

Methodologic Problems Encountered in the Assay of Proteinases in Lewis Lung Carcinoma, a Mouse Metastasizing Tumor

1982 ◽  
Vol 68 (5) ◽  
pp. 381-387 ◽  
Author(s):  
Tullio Giraldi ◽  
Gianni Sava ◽  
Marija Kopitar ◽  
Alois Suhar ◽  
Vito Turk ◽  
...  
Keyword(s):  
Proteolytic Activity ◽  
Lung Carcinoma ◽  
Lewis Lung Carcinoma ◽  
Tumor Tissue ◽  
Nuclear Extract ◽  
Cathepsin G ◽  
Normal Lung ◽  
Lewis Lung ◽  
Collagenase Activity ◽  
Whole Cells

The proteolytic activity in homogenates and extracts of subcellular fractions prepared from subcutaneous Lewis lung carcinoma was determined using proteins and synthetic peptides as substrates. The presence of cathepsin D, plasminogen activator, cathepsin B-, cathepsin G-and elastase-like enzymes was observed. No difference was revealed between the proteolytic activity in homogenates of Lewis lung carcinoma, at the growth stage examined, and in homogenates of normal lung. High specific activities were found in the lysosomal extract, whereas decreasing activities were found in the nuclear extract, the homogenate and the post-lysosomal mitochondrial supernatant; no active or trypsin-activatable collagenase activity was detected. The presence in the tumor tissue of these enzymatic activities is in agreement with their proposed role in the process of metastasis. The lack of differences between homogenates of tumor and normal lung tissue suggests that the use of whole cells is required to selectively study tumor proteinases specifically involved in tumor malignancy.

Human-specific c-neu proto-oncogene protein overexpression in human malignant astrocytomas before and after xenografting

1993 ◽  
Vol 78 (2) ◽  
pp. 240-251 ◽  
Author(s):  
Jerald J. Bernstein ◽  
Anna V. Anagnostopoulos ◽  
Emily A. Hattwick ◽  
Edward R. Laws
Keyword(s):  
Glial Fibrillary Acidic Protein ◽  
Tumor Tissue ◽  
Acidic Protein ◽  
Malignant Astrocytoma ◽  
Astrocytoma Cells ◽  
Hla Dr ◽  
Malignant Astrocytomas ◽  
Before And After ◽  
S 100 ◽  
Human Specific

✓ Overexpression of human-specific c-neu proto-oncogene transmembrane tyrosine kinase receptor protein (p185) is an index of cell transformation and of poor patient survival in several malignancies. The authors studied this protein in low- and high-grade human malignant astrocytomas before and after xenografting into aspiration pockets in rat cortex. Human-specific p185c-neu-positive cells were found in tumor specimens from all grades of astrocytoma. Significantly fewer p185c-neu-positive cells were observed in the low-grade versus the high-grade astrocytomas examined (p < 0.05). Human specific p185c-neu-positive cells were also positive for the human major histocompatibility complex, human leukocyte antigen (HLA)-DR, as well as glial fibrillary acidic protein and S-100 protein. Fresh suspensions of tumor tissue were prelabeled with the plant lectin Phaseolus vulgaris leukoagglutinin and xenografted into pockets in rat cortex. A class of human p185c-neu-positive cells found in tissue samples from all grades of astrocytoma migrated in the rat brain along parallel and intersecting nerve fiber bundles and basement membrane-lined surfaces. Migrated p185c-neu-positive cells were also positive for HLA-DR, Phaseolus vulgaris leukoagglutinin, glial fibrillary acidic protein, and S-100 protein, suggesting that they were in fact human astrocytoma cells. Simultaneous expression of human p185c-neu, HLA-DR, and glial fibrillary acidic protein was observed in a class of human malignant astrocytoma cells in both tumor tissue and xenografted cells that migrated into rat brain. These molecules are signature proteins for the study of the spread of human malignant astrocytomas in an animal model, and indicate that transformed human malignant astrocytoma cells can migrate within the parenchyma of the central nervous system and could play a role in the development of multifocal tumors.

Amyloid-β25–35 induces a permanent phosphorylation of HSF-1, but a transitory and inflammation-independent overexpression of Hsp-70 in C6 astrocytoma cells

Neuropeptides ◽  
2013 ◽  
Vol 47 (5) ◽  
pp. 339-346 ◽  
Author(s):  
Minerva Calvillo ◽  
Alfonso Diaz ◽  
Daniel I. Limon ◽  
Miguel Angel Mayoral ◽  
María Elena Chánez-Cárdenas ◽  
...  
Keyword(s):  
Hsp 70 ◽  
Astrocytoma Cells ◽  
C6 Astrocytoma

scholarly journals Effect of an Inhibitor of Lipid Peroxidation, U78517F, on C6 Astrocytoma Growth

1991 ◽  
Vol 18 (1) ◽  
pp. 7-11 ◽  
Author(s):  
Rolando F. Del Maestro ◽  
Christine R. Farrell ◽  
Eric Stroude ◽  
Warren McDonald
Keyword(s):  
Lipid Peroxidation ◽  
Tumor Growth ◽  
Monolayer Culture ◽  
Treatment Groups ◽  
Protein Extravasation ◽  
Astrocytoma Cell ◽  
C6 Astrocytoma ◽  
Post Implantation ◽  
Implantation Model

ABSTRACT:A potent in vitro inhibitor of lipid peroxidation, U78517F, has been employed to assess its influence on C6 astrocytoma growth in monolayer culture and tumor growth and protein extravasation in the rat C6 astrocytoma spheroid implantation model. Results demonstrate that 1 μM concentration of U78517F inhibits cell division, but is not tumoricidal to C6 astrocytoma cells in monolayer culture. Concentrations of 5 μM and above significantly decreased astrocytoma cell viability. Following spheroid implantation, rats were treated with one of these U785I7F regimes: 12 mg/kg/day for 13 days post-implantation, 4 mg/kg/day for 13 days post-implantation or 12 mg/kg/day commencing seven days post-implantation until 13 days post-implantation. Tumor wet and dry weights were lower in all treatment groups, but these decreases were not statistically significant. Protein extravasation as measured by Evans blue extravasation was not significantly reduced by any treatment regime used. It is concluded that U78517F inhibits C6 astrocytoma growth in monolayer culture at and above 5 μM concentrations, but the treatment regimes utilized did not significantly decrease tumor growth or permeability in the C6 astrocytoma spheroid implantation model.

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