scholarly journals Enamel Matrix Derivative and TGF-Beta 1 Target Genes in Human Tongue Carcinoma Cells

2020 ◽  
pp. 1-8
Author(s):  
Matti Mauramo ◽  
Matti Mauramo ◽  
Suvi-Tuuli Vilen ◽  
Timo Sorsa ◽  
Tuula Salo
Keyword(s):  
Transforming Growth Factor Beta ◽  
Target Genes ◽  
Transforming Growth Factor ◽  
Carcinoma Cells ◽  
Oral Carcinoma ◽  
Enamel Matrix Derivative ◽  
Enamel Matrix ◽  
Tgf Beta ◽  
Human Tongue ◽  
Matrix Derivative

Enamel matrix derivative (EMD) can enhance proliferation and migration of different oral cell lines, including malignant oral carcinoma cells, in vitro and in vivo. The composition of EMD is not known, but part of the effects have been postulated to be caused by transforming growth factor-beta-1 (TGF-beta 1). This study aimed to compare target genes of EMD and TGF-beta 1 on highly malignant oral carcinoma HSC-3 cells. Microarrays were used to examine differentially expressed genes in HSC-3 cells after 6h and 24h incubations with EMD (200 µg/ml) or TGF-beta 1 (10 ng/ml). Gene Ontology (GO) enrichment analysis of the regulated genes was also conducted. After 6h and 24h of EMD treatments 42 and 12 genes, respectively, were statistically significantly (P<0.05) up- or down-regulated. However, as many as 393 and 346 genes were statistically significantly (P<0.05) up- or down-regulated by TGF-beta 1. Among the most up-regulated genes by both of the study reagents were MMP-9 and -10. The expression of MMP-10 by EMD treated carcinoma cells was also verified in protein level. In conclusion, TGF-beta 1 regulates more and mostly different genes compared with EMD, but both regulate the expression of matrix metalloproteinase genes in oral carcinoma cells.

The enamel matrix derivative (Emdogain®) enhances human tongue carcinoma cells gelatinase production, migration and metastasis formation

Oral Oncology ◽  
2008 ◽  
Vol 44 (8) ◽  
pp. 733-742 ◽  
Author(s):  
Matti Laaksonen ◽  
Juho Suojanen ◽  
Sini Nurmenniemi ◽  
Esa Läärä ◽  
Timo Sorsa ◽  
...  
Keyword(s):  
Carcinoma Cells ◽  
Enamel Matrix Derivative ◽  
Tongue Carcinoma ◽  
Enamel Matrix ◽  
Metastasis Formation ◽  
Human Tongue ◽  
Matrix Derivative

scholarly journals Effects of enamel matrix derivative and transforming growth factor-β1 on human osteoblastic cells

2011 ◽  
Vol 7 (1) ◽  
Author(s):  
Daniela B. Palioto ◽  
Thaisângela L. Rodrigues ◽  
Julie T. Marchesan ◽  
Márcio M. Beloti ◽  
Paulo T. de Oliveira ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Osteoblastic Cells ◽  
Enamel Matrix Derivative ◽  
Enamel Matrix ◽  
Human Osteoblastic Cells ◽  
Matrix Derivative

Effects of enamel matrix derivative and transforming growth factor-?1 on human periodontal ligament fibroblasts

2007 ◽  
Vol 34 (6) ◽  
pp. 514-522 ◽  
Author(s):  
Thaisângela L. S. Rodrigues ◽  
Julie T. Marchesan ◽  
Ricardo D. Coletta ◽  
Arthur B. Novaes ◽  
Márcio F. de M. Grisi ◽  
...  
Keyword(s):  
Growth Factor ◽  
Periodontal Ligament ◽  
Transforming Growth Factor ◽  
Enamel Matrix Derivative ◽  
Enamel Matrix ◽  
Periodontal Ligament Fibroblasts ◽  
Human Periodontal Ligament Fibroblasts ◽  
Matrix Derivative

scholarly journals Regulation of the synthesis and activity of urokinase plasminogen activator in A549 human lung carcinoma cells by transforming growth factor-beta

1988 ◽  
Vol 106 (2) ◽  
pp. 451-459 ◽  
Author(s):  
J Keski-Oja ◽  
F Blasi ◽  
EB Leof ◽  
HL Moses
Keyword(s):  
Growth Factor ◽  
Lung Carcinoma ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Human Lung ◽  
A549 Cells ◽  
Carcinoma Cells ◽  
Tgf Beta ◽  
Lung Carcinoma Cells ◽  
Growth Factor Beta

Transforming growth factor-beta (TGF beta) is a regulator of cellular proliferation which can alter the proteolytic activity of cultured cells by enhancing the secretion of endothelial type plasminogen activator inhibitor and affecting the secretion of plasminogen activators (PAs) in cultured fibroblastic cells. We used the TGF beta-responsive malignant human lung adenocarcinoma cell line A549 to study the relationships between the known TGF beta-induced growth inhibition and the effects of TGF beta on the secretion of PA activity by A549 cells. PA activity was quantitated by caseinolysis assays, and characterized by urokinase mRNA analysis, immunoprecipitation, and zymography assays. PA-inhibitor production was observed in autoradiograms of SDS-polyacrylamide gels and reverse zymography assays. It was found that TGF beta enhanced the production of PA activity by these cells, in accordance with an enhancement of urokinase mRNA levels. A concomitant stimulation of type 1 PA-inhibitor production was also observed in A549 cells in response to TGF beta. In contrast to the observations of A549 cells, TGF beta caused a decrease in the expression of both urokinase and the tissue-type PA mRNA in human embryonic WI-38 lung fibroblasts indicating opposite regulation of the expression of PAs in these cells. The results suggest that TGF beta may play a role in the regulation of the invasive, proteolytically active phenotype of certain lung carcinoma cells.

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