Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.24.3 (collagenase)
 18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanism of albumin biosynthesis was studied in Morris hepatoma 5123tc in vivo and in hepatoma cell suspensions obtained by solubilizing the intercellular matrix with collagenase and hyaluronidase. In the in vivo experiments, L-[-14C]leucine was injected i.v. into rats bearing hepatomas in the muscles of both hind legs. After 14 min, tumors were removed and homogenized. A protein fraction quantitatively precipitable with antialbumin was isolated from the homogenate by acetone fractionation and precipitation with antiserum against serum albumin. This protein fraction was not homogeneous. With the use of 3 consecutive chromatographies on diethylaminoethyl cellulose, a very highly radioactive albumin-like protein could be separated from a large amount of only slightly radioactive albumin. In hepatoma cell suspensions incubated with L-[1-14C]leucine followed by a chase with excess nonradioactive L-leucine, radioactivity was incorporated first into the albumin-like protein and transferred thereafter into albumin, suggesting that albumin was synthesized via the albuminlike protein as precursor. In vivo, 1.8% of newly synthesized hepatoma protein was albumin or its precursor, compared with 1.2% in cell suspensions.
Cancer Res 1976 Sep
PMID:Biosynthesis of albumin via a precursor protein in Morris hepatoma 5123tc. 18 40

Normal and premalignant mouse mammary epithelial cells can be prepared in high yields by collagenase dissociation of minced glands followed by a brief, differential centrifugation to remove contaminating fibroblasts and fat cells. The major difficulties in preparing pure cultures in quantity are 1) incomplete dissociation of gland material, and 2) cell death during enzymatic digestion. These problems are eliminated by careful selection of collagenases for dissociation. Normal and premalignant mammary epithelial cells are morphologically indistinguishable from malignant mouse mammary epithelial cells in primary monolayer cultures. In addition, the growth rates and saturation densities achieved by normal mammary epithelial cells are indistinguishable from those of malignant mammary epithelial cells in primary culture. In both cases, a monolayer of cells is preserved with no evidence of focal overgrowth. Malignant adenocarcinoma mammary cells can however be distinguished from normal mammary epithelial cells by virtue of differences in their surface interactions with concanavalin A. A hemadsorption assay using Con-A-coated erythrocytes was the most sensitive indicator for these differences. In hemadsorption assays malignant mammary epithelial cells were half-maximally reactive with 2.5 mug/ml concanavalin A, while normal cells were completely unreactive even at concanavalin A concentrations five-times higher. Premalignant mammary epithelial cells were as reactive as malignant mammary epithelial cells in the hemadsorption assays. Hemadsorption of malignant cells was observed in primary and secondary cultures of epithelium as well as in cell lines. Malignant cells forming mammary adenocarcinomas were as highly reactive as malignant cells forming scirrhous carcinomas. Malignant cells not releasing mammary tumor virus (MuMTV) were as reactive as cells releasing that virus. Adsorption of concanavalin-A-coated erythrocytes to normal mammary epithelial cells could be induced by brief treatment of cell monolayers with hyaluronidase. Exposure of active sites was not affected with either trypsin or collagenase. Our results show that while the growth of malignant cells does not serve to distinguish them from normal cells in monolayer culture, surface changes do exist which can be identified by differences in concanavalin A reactivity. Since the earliest transformants identifiable in vivo (premalignant) have undergone conversion of the surface marker, concanavalin-A-mediated hemadsorption provides a sensitive measure for mammary epithelial cell transformants in vitro.
Int J Cancer 1976 Oct 15
PMID:Markers to distinguish normal and neoplastic mammary epithelial cells in vitro: comparison of saturation density, morphology and concanavalin A reactivity. 18 59

Gonadotropic hormones are required for the induction and maintenance of tumors arising in ovaries that have been transplanted to the spleens of gonadectomized mice. The characteristics of gonadotropin receptors for human chorionic gonadotropin (HCG)-luteinizing hormone on cells from these tumors of varying size, age, and morphology have been determined. The specific binding of 125I-labeled HCG to cells obtained by collagenase digestion, 15 to 65 weeks postimplantation from granulosa cell or luteinized cell, or mixed granulosa-luteal tumors was analyzed by Scatchard plot. Neither the size, weight, duration of implantation, nor histological morphology affected the receptor-binding affinity [equilibrium dissociation constant (Kd), 6 X 10(-10) M], and, presumably, the receptor is qualitatively similar. In contrast, the number of HCG receptors per cell increased 17-fold and was related to the degree of morphological luteinization of the tumor. HCG-sensitive adenyl cyclase was also demonstrated and compared to HCG binding in a highly luteinized tumor.
Cancer Res 1977 Aug
PMID:Gonadotropin receptors in experimentally induced ovarian tumors in mice. 19 83

Samples of 35 tumors from the head and neck region (25 squamous cell, 2 basal cell, 5 parotid, 3 melanoma, and 1 lymphosarcoma) were cultured after dispersement with either trypsin or collagenase treatment. Growth was established in 14 (40%). Cultured tumor cells were then used as target cells in in vitro assays of patients' cellular and humoral immunity to their own or similar tumors. Preliminary data suggest this may be a reliable method of monitoring responses in patients receiving immunotherapy for head and neck malignancies.
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PMID:Tissue-cultured head and neck tumors: their use in in vitro assays of immune response. 19 78

Preneoplastic mammary nodule lines D1, D2, and C4 were enzymatically dissociated with collagenase, hyaluronidase, and pronase or with only collagenase and hyaluronidase to produce high yields of viable single cells; 10(5) cells were injected into the cleared mammary fat pads of syngeneic BALB/cCrgl mice. In 11 experiments involving three different preneoplastic nodule lines with different tumor potentials, all dissociated nodule cell lines showed a marked increase in tumorigenicity as compared to the same tissues transplanted as 1-mm3 pieces. The results could not be explained on the basis of differences between the amounts of cells transplanted in the two procedures. In a second series of experiments, normal mammary cells from virgin, pregnant, or lactating mice were mixed in different ratios with 10(5) nodule cells and injected into the mammary fat pads. The presence of normal cells reversed the marked increase in the tumorigenicity of enzymatically dissociated nodule cells to a level equal to or less than the tumorigenicity of control transplants (1-mm3 pieces). The growth of 10(5) mammary tumor cells was not inhibited when tumor cells were mixed with 3 x 10(5) normal cells and transplanted into the mammary fat pads. These results showed that enzymatic dissociation can lead to an increase in tumor potential of preneoplastic mammary nodule lines, and they supported the hypothesis that nodule cells, but not neoplastic cells, are sensitive to the growth-inhibitory effects of normal mammary cells.
J Natl Cancer Inst 1978 May
PMID:Enhancement of the tumorigenicity of preneoplastic mammary nodule lines by enzymatic dissociation. 20 61

Inapparent nodule-transformed cells were recovered from morphologically normal mammary tissue from virgin female BALB/cfC3H/Crgl (mouse mammary tumor-positive) mice before the appearance of hyperplastic alveolar nodules (HAN) or tumors, by means of the cell dissociation technique. Mammary tissues were dissociated by means of collagenase (0.1%), hyaluronidase (0.1%), and pronase (1.25%). Aliquots of 10(5) viable cells in 0.01 ml medium were injected into the gland-free mammary fat pads of 3-week-old female syngeneic mice. After 10 weeks the outgrowths were examined and classified as ductal, HAN, tumor, or combinations of these types. The presence of HAN outgrowths indicated the presence of nodule-transformed cells in the donor mammary tissues. Nodule-transformed cells were recovered from 2-month-old donors, and the number of HAN outgrowths increased with donor age. Overt HAN and tumors did not appear in virgin female BALB/cfC3H/Crgl mice younger than 8 to 9 months of age. The data suggest that inapparent nodule-transformed cells occurred long before the appearance of HAN of tumors and that the numbers of transformed cells increased with donor age.
Cancer Res 1978 Jul
PMID:Detection of inapparent nodule-transformed cells in the mammary gland tissues of virgin female BALB/cfC3H mice. 20 23

The effect of the potent tumor promoter phorbol 12-myristate 13-acetate (PMA) on collagen synthesis, a differentiated property of chick embryo fibroblasts, was examined. Collagen synthesis, as measured by the rate of formation of [3H]hydroxyproline from [3H]proline, was found to be decreased in cells treated with PMA but not in cells treated with the parent alcohol phorbol. The decrease in collagenase-sensitive proteins was confirmed by polyacrylamide gel electrophoresis of cell lysates, indicating that the decrease could not be ascribed simply to an effect on prolyl hydroxylase. Although a decrease in collagen synthesis was observed after one day, five days were required for a maximal reduction to 20% of that of dimethyl sulfoxide-treated controls. The effect of PMA on collagen synthesis was reversible. It was therefore not the result of a permanent transformation of the cells or of the selection of a population of cells with a reduced capacity for collagen synthesis. Collagen synthesis was decreased in chick embryo fibroblasts transformed by Rous sarcoma virus. Treatment of these cells with PMA for 5 days brought about a further decrease to 50% of the level in dimethyl sulfoxide-treated transformed controls.
Cancer Res 1979 May
PMID:Decrease in collagen production in normal and Rous sarcoma virus-transformed chick embryo fibroblasts induced by phorbol myristate acetate. 21 32

Fibroblast cultures derived from human basal cell carcinomas demonstrated an increased capacity to synthesize and secrete collagenase. Although the levels of collagenase were up to 8-fold greater than those of normal control cell lines, this phenotypic trait was not permanent and was expressed only for a few passages following primary explanation. The basal cell carcinoma fibroblast collagenase was secreted as a proenzyme. The kinetics of activation and the catalytic efficiency of the basal cell carcinoma fibroblast enzyme were equal to control collagenase, indicating that increased activity was due to increased synthesis of enzyme protein. Increased synthesis of collagenase was not due either to altered cell growth or to an overall increase in protein synthesis. Furthermore, synthesis of another major protein, of another major protein, collagen, was not enhanced. The data suggest that the tumors may have stimulated adjacent fibroblasts to produce more collagenase which is of importance in tumor invasion.
Cancer Res 1979 Nov
PMID:Enhanced collagenase production by fibroblasts derived from human basal cell carcinomas. 22 89

Solid human tumors were dissociated with collagenase, cultured for 16-48 hours, and harvested for cytogenetic preparation. Of the 19 tumors used, 14 showed sufficient numbers of metaphases to be useful for chromosome analysis.
J Natl Cancer Inst 1979 Nov
PMID:Improved method for cytogenetic studies of solid tumors. 22 4

The concanavalin A (Con A)-induced agglutinability of normal, preneoplastic, and neoplastic mouse mammary epithelial cells was examined. Cells freshly dissociated from normal mammary glands, hyperplastic alveolar nodules, or primary mammary adenocarcinomas by collagenase digestion in the presence of bovine serum albumin were strongly agglutinated by low concentrations of Con A. After short-term culture in vitro, however, cells from all three types of tissue were only weakly agglutinated by Con A, as measured by both suspension and hemadsorption assays. By comparison, cells of three established mammary tumor culture lines agglutinated strongly in the presence of the lectin. Treatment of the normal, preneoplastic, and neoplastic mammary cells in primary cultures with either trypsin or collagenase had little or no effect on their agglutinability, whereas hyaluronidase significantly increased their reactivity. Studies with fluorescein-tagged Con A indicated that all three cell types were capable of binding the lectin. The results were consistent with previous evidence suggesting that neoplastic transformation of mouse mammary epithelial cells is not manifested in vitro by several of the alterations in growth patterns, intercellular interactions, and surface properties that usually accompany transformation of fibroblastic cells.
J Natl Cancer Inst 1978 Dec
PMID:Concanavalin A-induced agglutinability of normal, preneoplastic, and neoplastic mouse mammary cells. 28 51


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