Overexpression of nPKCδ in BL6 murine melanoma cells enhances TGFβ1 release into the plasma of metastasized animals
Autor: | C. A. M. La Porta, Roberto Comolli |
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Rok vydání: | 2000 |
Předmět: |
Gene isoform
Cancer Research Lung Neoplasms Angiogenesis medicine.medical_treatment Blotting Western Dermatology Metastasis Transforming Growth Factor beta1 Mice Transforming Growth Factor beta Tumor Cells Cultured medicine Animals Protein Isoforms Neoplasm Metastasis Melanoma Protein Kinase C Protein kinase C Lung Neovascularization Pathologic Reverse Transcriptase Polymerase Chain Reaction Chemistry Immunosuppression medicine.disease Immunohistochemistry biological factors Isoenzymes Mice Inbred C57BL Protein Kinase C-delta Cytokine medicine.anatomical_structure Oncology embryonic structures Cancer research Neoplasm Transplantation Densitometry Signal Transduction |
Zdroj: | Melanoma Research. 10:527-534 |
ISSN: | 0960-8931 |
DOI: | 10.1097/00008390-200012000-00003 |
Popis: | Transforming growth factor-beta (TGFbeta) contributes to the promotion of invasion, metastasis, angiogenesis and even immunosuppression. Since overexpression of the delta isoform of protein kinase C (nPKCdelta) in BL6 murine melanoma cells (BL6T cells) increases their metastatic capacity, we investigated the possible involvement of TGFbeta1 in this process. Immunohistochemical analysis demonstrated lower levels of TGFbeta1 in BL6T lung metastases compared with BL6 lung metastases. On the other hand, higher levels of this cytokine, in particular in its active form, occur in the plasma of BL6T metastasized animals, suggesting a nPKCdelta-dependent TGFbeta1 release. Therefore, nPKCdelta-dependent TGFbeta1 release and activation may be involved in the greater angiogenic and metastatic capacity of murine melanoma BL6T cells. |
Databáze: | OpenAIRE |
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