Antisense-mediated reduction in thrombospondin reverses the malignant phenotype of a human squamous carcinoma.

@article{Castle1991AntisensemediatedRI,
  title={Antisense-mediated reduction in thrombospondin reverses the malignant phenotype of a human squamous carcinoma.},
  author={Valerie P. Castle and James Varani and Suzanne E. G. Fligiel and Edward V. Prochownik and Vishva M. Dixit},
  journal={The Journal of clinical investigation},
  year={1991},
  volume={87 6},
  pages={
          1883-8
        }
}
Thrombospondin (TSP) is a trimeric glycoprotein which is synthesized and incorporated into the extracellular matrix by a wide variety of cells. TSP is involved in a number of cellular processes which govern tumor cell behavior including mitogenesis, attachment, migration, and differentiation. To directly assess the role of TSP in tumor cell growth and spread, a human squamous carcinoma cell line, with high TSP production and an invasive phenotype, was transfected with a TSP cDNA antisense… 
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Overexpression of thrombospondin-1 decreases angiogenesis and inhibits the growth of human cutaneous squamous cell carcinomas.
Expression of the thrombospondin 1 fragment 167–569 in C6 glioma cells stimulates tumorigenicity despite reduced neovascularization
TLDR
The results indicate that careful attention should be paid at designing smaller fragments from the multimodular angiostatic molecule TSP1 since, as observed in this study, it may unmask protumorigenic properties that counteract its antiangiogenic activity.
Antisense‐mediated reduction in thrombospondin‐1 expression reduces cell motility in malignant glioma cells
TLDR
Transfection of TSP‐1 complementary deoxyribonucleic acid sense and antisense expression vectors into the glioblastoma cell line T98G‐G7 suggests that TSP•1 secreted by malignant glioma cells is involved in the motility of gliomas cells.
Thrombospondin-1 enhances human thyroid carcinoma cell invasion through urokinase activity.
Adenovirus-mediated gene therapy with an antiangiogenic fragment of thrombospondin-1 inhibits human leukemia xenograft growth in nude mice.
Transformation by v-src causes transient induction followed by repression of mouse thrombospondin-1.
  • J. Slack, P. Bornstein
  • Biology
    Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research
  • 1994
TLDR
The ultimate result of v-src transformation, at least in rodent fibroblasts, is repression of TSP-1 gene expression, as determined by nuclear run-on assays.
Regulation of tumor growth and metastasis by thrombospondin‐1
  • D. Roberts
  • Biology
    FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • 1996
TLDR
Relating these phenom‐ena to the molecular interactions of TSP1 observed in vitro may lead to novel therapeutic strategies for controlling cancer progression and metastasis.
Thrombospondin modulates human breast adenocarcinoma cell adhesion to human vascular endothelial cells.
TLDR
Results indicate that mammary adenocarcinoma cells use TSP to form aggregates and to attach to human endothelial cells, which may have physiological implications during the hematogenous spread of tumor cells.
Involvement of thrombospondin in the adherence of human breast‐adenocarcinoma cells: A possible role in the metastatic process
TLDR
Endogenously synthesized thrombospondin (TSP) may have a role in the cyto‐adherence of tumor cells during the spread of breast cancer.
Tumor suppression in human skin carcinoma cells by chromosome 15 transfer or thrombospondin-1 overexpression through halted tumor vascularization.
TLDR
Thrombospondin-1 is strongly suggested as a potential tumor suppressor on chromosome 15, which acts as a matrix barrier at the tumor/stroma border, which, by halting tumor vascularization, prevents tumor cell invasion and, thus, tumor expansion.
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