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Invasion & metastasis最新文献

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Antimetastatic effect of PSK, a protein-bound polysaccharide, against the B16-BL6 mouse melanoma. 蛋白结合多糖PSK对B16-BL6小鼠黑色素瘤的抗转移作用。
Invasion & metastasis Pub Date : 1996-01-01
K Matsunaga, M Ohhara, Y Oguchi, H Iijima, H Kobayashi
{"title":"Antimetastatic effect of PSK, a protein-bound polysaccharide, against the B16-BL6 mouse melanoma.","authors":"K Matsunaga,&nbsp;M Ohhara,&nbsp;Y Oguchi,&nbsp;H Iijima,&nbsp;H Kobayashi","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We examined the effect of PSK, a protein-bound polysaccharide, upon in vivo metastasis and in vitro invasion of the B16-BL6 mouse melanoma cells. (1) PSK suppressed in vivo artificial and spontaneous lung metastases of B16-BL6 in C57BL/6 mice. (2) PSK in a dose-dependent fashion suppressed in vitro invasion and chemotaxis of the tumor cells using filters coated with a reconstituted basement membrane. (3) PSK had little effect on DNA synthesis in tumor cells in vitro, but suppressed tumor cell adhesion to, degradation of, and haptotaxis to components of the basement membrane. (4) PSK suppressed the binding of tumor cells to components of the basement membrane. These findings suggest that PSK may suppress metastasis through inhibition of tumor cell invasion and that this effect is the result of interactions between PSK and components of the basement membrane.</p>","PeriodicalId":14452,"journal":{"name":"Invasion & metastasis","volume":"16 1","pages":"27-38"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19799075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Membrane-type matrix metalloproteinase expression and matrix metalloproteinase-2 activation in primary human ovarian epithelial carcinoma cells. 膜型基质金属蛋白酶的表达及基质金属蛋白酶-2在人卵巢上皮癌细胞中的活化。
Invasion & metastasis Pub Date : 1996-01-01
D A Fishman, L M Bafetti, M S Stack
{"title":"Membrane-type matrix metalloproteinase expression and matrix metalloproteinase-2 activation in primary human ovarian epithelial carcinoma cells.","authors":"D A Fishman,&nbsp;L M Bafetti,&nbsp;M S Stack","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Metastatic dissemination of epithelial ovarian carcinoma occurs primarily through exfoliation of cells from the primary tumor, with subsequent implantation, invasion, and growth throughout the organs within the peritoneal cavity. Previous studies have suggested a role for matrix metalloproteinases (MMPs), particularly MMP-2, in ovarian cancer invasion and metastasis. To characterize further the role of MMPs and their inhibitors in ovarian carcinoma, in this study the production and activation of MMPs by short-term primary cultures of human ovarian epithelial carcinoma cells were analyzed. We report that MMP-2 is the predominant gelatinolytic MMP secreted by primary ovarian cancer cells derived from both ovarian tumors and ascites fluid. Furthermore, zymographic analysis demonstrated that MMP-2 is present in conditioned media in both the latent and activated forms, indicating that primary ovarian cancer cells catalyze proMMP-2 activation. Presence of a proMMP-2 activator was confirmed by immunohistochemistry and immunoprecipitation studies which found membrane-type 1 MMP (MT1-MMP) in the membranes of unstimulated cells and levels of both MT1-MMP and tissue inhibitor of metalloproteinases-2 (TIMP-2) were enhanced by culturing cells in the presence of concanavalin A. In addition, interaction of MMP-2 with the ovarian carcinoma cell surface resulted in a 2.5- to 5-fold increase in invasiveness. These data suggest that MT1-MMP-catalyzed activation of proMMP-2 may play a physiologic role in intraperitoneal invasion of ovarian carcinoma cells.</p>","PeriodicalId":14452,"journal":{"name":"Invasion & metastasis","volume":"16 3","pages":"150-9"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20132569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Potential role of platelets and coagulation factors in the metastasis of prostatic cancer. 血小板和凝血因子在前列腺癌转移中的潜在作用。
Invasion & metastasis Pub Date : 1996-01-01
R A Bhatti, J Gadarowski, P Ray
{"title":"Potential role of platelets and coagulation factors in the metastasis of prostatic cancer.","authors":"R A Bhatti,&nbsp;J Gadarowski,&nbsp;P Ray","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>One of the common surgical procedures used in the management of prostate cancer is transurethral resection of the prostate in which the possibility of the escape of tumor cells and their encounter with the hemostatic system is reported to contribute to the threat of hematogenous dissemination. We are reporting about the role of the hemostatic system involving the platelets and coagulation factors in the dissemination process in a tumor model carrying Dunning's R3327 AT3 adenocarcinoma of the prostate whose metastatic behavior is similar to that of human prostatic cancer. Our data revealed that the number of circulating platelets dropped and their aggregation activity increased in tumor-bearing rats as compared to controls. Normal platelets when treated with tumor effusions and reacted with the exogenous aggregating agent collagen exhibited a significant increase in the aggregating activity suggesting that the tumor and its microenvironment were capable of activating the hemostatic system. Out of eight coagulation factors measured only factors XI and XII were significantly decreased in tumor-bearing rats. The role of platelets in the metastatic process is discussed.</p>","PeriodicalId":14452,"journal":{"name":"Invasion & metastasis","volume":"16 2","pages":"49-55"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19989898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Biological inferences from a mathematical model for malignant invasion. 恶性侵袭的数学模型的生物学推论。
Invasion & metastasis Pub Date : 1996-01-01
A J Perumpanani, J A Sherratt, J Norbury, H M Byrne
{"title":"Biological inferences from a mathematical model for malignant invasion.","authors":"A J Perumpanani,&nbsp;J A Sherratt,&nbsp;J Norbury,&nbsp;H M Byrne","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Invasive cells show changes in adhesion, motility and the protease-antiprotease balance. In this paper the authors derive a model based on a continuum approach that describes the behaviour of the invasive cells. The invasive cells are studied in the context of their interaction with normal cells, noninvasive tumour cells, ECM proteins and the proteases. The authors briefly describe the methods of mathematical analysis used and then go on to highlight the biological inferences drawn from the mathematical analysis. Based on the results from the modelling the authors suggest that the movement of cells under the simultaneous effects of a haptotactic gradient and a concomitantly created chemotactic gradient is oscillatory both with respect to the speed of invasion and the wave profile of the invasive cells. They further demonstrate that the average speed of invasion can be computed as a measure of the phenotypic properties of the cell and the matrix. They use the model to suggest an intuitive explanation for the occurrence of noninvasion with high protease expression on the basis of chemotactic gradients that prevent invasion. The authors have studied the effect of the diffusivity of the protease on an invading cell and shown that increase in diffusivity initially results in enhanced invasion, but extreme increases in protease diffusivity can result in noninvasion.</p>","PeriodicalId":14452,"journal":{"name":"Invasion & metastasis","volume":"16 4-5","pages":"209-21"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20249890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Inhibition of lymphatic metastasis in a syngeneic rat fibrosarcoma model by an angiogenesis inhibitor, AGM-1470. 血管生成抑制剂AGM-1470对同基因大鼠纤维肉瘤淋巴转移的抑制作用
Invasion & metastasis Pub Date : 1996-01-01
H Futami, H Iseki, S Egawa, K Koyama, K Yamaguchi
{"title":"Inhibition of lymphatic metastasis in a syngeneic rat fibrosarcoma model by an angiogenesis inhibitor, AGM-1470.","authors":"H Futami,&nbsp;H Iseki,&nbsp;S Egawa,&nbsp;K Koyama,&nbsp;K Yamaguchi","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We examined whether lymphatic metastasis was inhibited by the potent angiogenesis inhibitor AGM-1470 [O-(chloroacetyl-carbamoyl)fumagillol, TNP-470] using a rat lymphatic metastasis model. Clone A of the rat fibrosarcoma AS653HM, when inoculated into the footpads of syngeneic rats, highly and preferentially metastasized to lymph nodes. In contrast, when AGM-1470 was administered subcutaneously to rats bearing the tumor cells, the tumor growth and incidence of metastasis in the lymph nodes were reduced in a dose- and schedule-dependent manner. Similar inhibition of lymphatic metastasis was also observed in the rats in which treatment with AGM-1470 was initiated following resection of the primary tumor in the foot, indicating that the treatment with AGM-1470 inhibited the progression of lymphatic metastasis at the metastatic sites of the lymph nodes. These results suggest that AGM-1470 can be a potential agent to prevent lymphatic metastasis.</p>","PeriodicalId":14452,"journal":{"name":"Invasion & metastasis","volume":"16 2","pages":"73-82"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19989901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Metastatic human rhabdomyosarcoma: molecular, cellular and cytogenetic analysis of a novel cellular model. 转移性人横纹肌肉瘤:一种新型细胞模型的分子、细胞和细胞遗传学分析。
Invasion & metastasis Pub Date : 1996-01-01
T Kalebic, J G Judde, M Velez-Yanguas, T Knutsen, L J Helman
{"title":"Metastatic human rhabdomyosarcoma: molecular, cellular and cytogenetic analysis of a novel cellular model.","authors":"T Kalebic,&nbsp;J G Judde,&nbsp;M Velez-Yanguas,&nbsp;T Knutsen,&nbsp;L J Helman","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A new human metastatic rhabdomyosarcoma (RMS) model was established and analyzed for a number of biologic, cytogenetic and molecular parameters. Consistent with previous studies, the metastatic capacity of different RMS cell variants did not correlate with their tumorigenic or proliferative capacities. Interestingly, a highly metastatic variant was diploid, while a nonmetastatic variant was tetraploid, which parallels previous clinical observations. Genes whose expression had been found to be associated with either low- or high-metastatic capacity in carcinoma or melanoma did not show a similar association with different metastatic variants of RMS, derived from a mesenchymal tumor. We also found, in transient reporter gene assays, that several promoters had higher transcriptional activity in highly metastatic than in nonmetastatic RMS cell variants. This novel human RMS metastatic model may be instrumental for a better understanding of the regulatory pathways that control the metastatic phenotype of tumors of mesenchymal origin.</p>","PeriodicalId":14452,"journal":{"name":"Invasion & metastasis","volume":"16 2","pages":"83-96"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19989902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Tumor heterogeneity and progression: conceptual foundations for modeling. 肿瘤异质性和进展:模型的概念基础。
Invasion & metastasis Pub Date : 1996-01-01
L D Greller, F L Tobin, G Poste
{"title":"Tumor heterogeneity and progression: conceptual foundations for modeling.","authors":"L D Greller,&nbsp;F L Tobin,&nbsp;G Poste","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A conceptual foundation for modeling tumor progression, growth, and heterogeneity is presented. The purpose of such models is to aid understanding, test ideas, formulate experiments, and to model cancer 'in machina' to address the dynamic features of tumor cell heterogeneity, progression, and growth. The descriptive capabilities of such an approach provides a consistent language for qualitatively reasoning about tumor behavior. This approach provides a schema for building conceptual models that combine three key phenomenological driving elements: growth, progression, and genetic instability. The growth element encompasses processes contributing to changes in tumor bulk and is distinct from progression per se. The progression element subsumes a broad collection of processes underlying phenotypic progression. The genetics elements represents heritable changes which potentially affect tumor character and behavior. Models, conceptual and mathematical, can be built for different tumor situations by drawing upon the interaction of these three distinct driving elements. These models can be used as tools to explore a diversity of hypotheses concerning dynamic changes in cellular populations during tumor progression, including the generation of intratumor heterogeneity. Such models can also serve to guide experimentation and to gain insight into dynamic aspects of complex tumor behavior.</p>","PeriodicalId":14452,"journal":{"name":"Invasion & metastasis","volume":"16 4-5","pages":"177-208"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20249889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
In vivo binding of the radioiodinated peptide YIGSR on B16 melanoma cells. 放射性碘化肽YIGSR在B16黑色素瘤细胞上的体内结合。
Invasion & metastasis Pub Date : 1996-01-01
K Kouzi-Koliakos, G Koliakos, C Trontzos, A Papageorgiou, S Iliadis, A Triantos, A Dimitriadou, M Kanellaki
{"title":"In vivo binding of the radioiodinated peptide YIGSR on B16 melanoma cells.","authors":"K Kouzi-Koliakos,&nbsp;G Koliakos,&nbsp;C Trontzos,&nbsp;A Papageorgiou,&nbsp;S Iliadis,&nbsp;A Triantos,&nbsp;A Dimitriadou,&nbsp;M Kanellaki","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>It has been reported that metastatic melanoma cell lines selectively bind in vitro with the synthetic laminin pentapeptide tyrosyl-isoleucyl-glycyl-seryl-arginine (YIGSR). The aim of this study was to investigate whether the same peptide can bind on melanoma cells in vivo as well. Iodine-125-labeled YIGSR was administered to B16 melanoma-bearing animals. Microscopic autoradiography of tumor and organ sections taken 24 h after peptide administration showed that the peptide did accumulate on the surface of certain tumor cells. The peptide binding cells were frequent in metastatic sites and tumors grown for 24 days and rare in tumors grown for 10 days. A similarly radiolabeled control pentapeptide (peptide DRLKY) did not bind to any tumor cell. It is suggested that the YIGSR binding tumor cells may represent a distinct melanoma cell population with a high metastatic potential.</p>","PeriodicalId":14452,"journal":{"name":"Invasion & metastasis","volume":"16 6","pages":"322-9"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20301708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The lac-z reporter gene: a tool for in vitro studies of malignant glioma cell invasion. lac-z报告基因:恶性胶质瘤细胞侵袭体外研究的工具。
Invasion & metastasis Pub Date : 1996-01-01
I Garcia-Cabrera, K Edvardsen, B B Tysnes, T Read, R Bjerkvig
{"title":"The lac-z reporter gene: a tool for in vitro studies of malignant glioma cell invasion.","authors":"I Garcia-Cabrera,&nbsp;K Edvardsen,&nbsp;B B Tysnes,&nbsp;T Read,&nbsp;R Bjerkvig","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A reporter gene (lac-z) was introduced into rat (BT4C) and human (D-54 MG) proliferating glioma cell lines by means of liposomal transfection. Lac-z-transfected glioma cells were first cultured as multicellular spheroids and then confronted with fetal brain aggregates. After various intervals the lac-z reporter gene product, bacterial beta-galactosidase, was histochemically detected in the cocultures. beta-Galactosidase was only detected in the glioma cells which showed an intense blue staining, which made them easily distinguishable from fetal tissue. Both glioma cell lines showed a clear pattern of migration and increasing invasion with time as the tumor cells infiltrated and destroyed the brain aggregates. Spheroid growth curves showed no significant differences between transfected and nontransfected cell lines. Likewise, flow cytometry measurements revealed no significant changes in ploidy between transfected and nontransfected rat glioma cells. In comparison, a shift in ploidy was observed in the human glioma cells after lac-z transfection. Stable integration of the lac-z gene into tumor cells was verified by Southern blot analysis. The results indicate that transfection of the lac-z reporter gene into glioma cells lines does not affect their growth or invasion potential in vitro. The lac-z reporter gene can thus be exploited to facilitate visualization of single migrating tumor cells and quantification of tumor invasion in in vitro coculture systems.</p>","PeriodicalId":14452,"journal":{"name":"Invasion & metastasis","volume":"16 3","pages":"107-15"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20133256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Defective tumor vascularization induced by metastasin 1 expression. 转移蛋白1表达诱导肿瘤血管化缺陷。
Invasion & metastasis Pub Date : 1996-01-01
A Onischenko, M P Chenard, O Lefebvre, E Bruyneel, M C Rio
{"title":"Defective tumor vascularization induced by metastasin 1 expression.","authors":"A Onischenko,&nbsp;M P Chenard,&nbsp;O Lefebvre,&nbsp;E Bruyneel,&nbsp;M C Rio","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>It has been proposed that metastasin 1 (mts1), a member of the S100 Ca(2+)-binding protein family, may play a role in tumor progression and metastasis. In order to test this possibility, we have performed gene transfer experiments using a human sense mts1 expression vector and human MCF7 malignant epithelial cells which do not express endogenous mts1. In vitro, mts1 expression did not modify proliferative or invasive properties of transfected MCF7 cells. In vivo, MCF7 cells expressing mts1 were associated with tumors exhibiting necrosis, and abundant fibrous and poorly cellular stroma. Immunohistochemical staining of endothelial cells showed that, in the presence of mts1, the number and the size of tumoral microvessels were decreased and some of them were collapsed. No metastases were observed in mice with either mts1-expressing or nonexpressing tumors. In summary, these results indicate that (i) in vitro and in vivo, mts1 does not confer invasive properties to MCF7 cells, and (ii) mts1 expression by MCF7 cells leads to defective tumor microvessels, leading to the hypothesis that mts1 may have a negative effect on neoangiogenesis and/or on the maintenance of blood vessels.</p>","PeriodicalId":14452,"journal":{"name":"Invasion & metastasis","volume":"16 3","pages":"160-8"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20132570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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