scholarly journals The Importance of Growth Factors and Steroid Hormones in Ovarian Cancer

Onkologie ◽  
2009 ◽  
Vol 32 (11) ◽  
pp. 623-624 ◽  
Author(s):  
Simon P. Langdon ◽  
Dana Faratian ◽  
David J. Harrison
Keyword(s):  
Ovarian Cancer ◽  
Growth Factors ◽  
Steroid Hormones

Steroid-induced cell proliferation in vivo is associated with increased c-myc proto-oncogene transcript abundance

Development ◽  
1988 ◽  
Vol 104 (1) ◽  
pp. 87-95
Author(s):  
S.A. Rempel ◽  
R.N. Johnston
Keyword(s):  
Cell Proliferation ◽  
Growth Factors ◽  
Steroid Hormones ◽  
Steroid Hormone ◽  
Normal Liver ◽  
Transcript Abundance ◽  
Chicken Oviduct ◽  
Massive Cell ◽  
In Cells

Enhanced c-myc transcript abundance has been observed in a variety of human malignancies, in normal liver tissue induced to proliferate in vivo by partial hepatectomy and in cells in culture induced to proliferate with the addition of protein hormones and growth factors. Little is known, however, about the expression of cellular proto-oncogenes in cells induced to proliferate in vivo by steroid hormones. Experiments reported here indicate that when cells of the immature chicken oviduct are induced to undergo rapid in vivo proliferation by application of the estrogen hormone 17 beta-estradiol, the onset of this proliferation is associated with a rapid, large, and transient increase in c-myc transcript abundance. When estrogen is administered to chickens in which the oviduct has already differentiated, neither massive cell proliferation nor large increases in c-myc transcript abundance are induced. We conclude that the abundance of c-myc transcripts in vivo correlates well with the degree of cell proliferation induced by steroid hormone.

Steroid Hormones and Growth Factors Act in an Integrated Manner at the Levels of Hypothalamic Astrocytes

2003 ◽  
Vol 1007 (1) ◽  
pp. 162-168 ◽  
Author(s):  
MARIARITA GALBIATI ◽  
SIMONA SAREDI ◽  
ROBERTO C. MELCANGI
Keyword(s):  
Growth Factors ◽  
Steroid Hormones

Growth factors and ovarian cancer

1998 ◽  
Vol 5 (4) ◽  
pp. 283-291 ◽  
Author(s):  
S P Langdon
Keyword(s):  
Ovarian Cancer ◽  
Growth Factors

Steroid Hormones and Growth Factors in Breast Cancer

1990 ◽  
Vol 595 (1 Steroid Forma) ◽  
pp. 236-241 ◽  
Author(s):  
Robin Leake ◽  
David Kerr ◽  
Frank Rinaldi
Keyword(s):  
Breast Cancer ◽  
Growth Factors ◽  
Steroid Hormones

Urinary excretion of growth factors in patients with ovarian cancer

1994 ◽  
Vol 30 (12) ◽  
pp. 1851-1858 ◽  
Author(s):  
M. Feldkamper ◽  
U. Enderle-Schmitt ◽  
R. Hackenberg ◽  
K.-D. Schulz
Keyword(s):  
Ovarian Cancer ◽  
Growth Factors ◽  
Urinary Excretion

Growth factors in human ovarian cancer

1997 ◽  
Vol 23 (2) ◽  
pp. 113-131 ◽  
Author(s):  
A.M. Westermann ◽  
J.H. Beijnen ◽  
W.H. Moolenaar ◽  
S. Rodenhuis
Keyword(s):  
Ovarian Cancer ◽  
Growth Factors ◽  
Human Ovarian Cancer

scholarly journals Co-Activation of TGFβ and Wnt Signalling Pathways Abrogates EMT in Ovarian Cancer Cells

2017 ◽  
Vol 41 (4) ◽  
pp. 1336-1345 ◽  
Author(s):  
Tulika Mitra ◽  
Sib Sankar Roy
Keyword(s):  
Ovarian Cancer ◽  
Growth Factors ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Wnt Signalling ◽  
Luciferase Assay ◽  
Signalling Pathways ◽  
Ovarian Cancer Cells ◽  
Mesenchymal Transition ◽  
Co Activation

Background/Aims: The aggressive property of ovarian cancer (OC) in terms of epithelial-mesenchymal transition (EMT), proliferation and metastasis are of major concern. Different growth factors including TGFβ are associated with regulating these molecular events but the underlying mechanisms remain unclear. The aim of this report is to decipher the regulation of EMT by co-activation of TGFβ and Wnt signalling cascades in gaining malignancy. Methods: The expression of the different components of signalling events were analyzed by QPCR, Western blot, Immunofluorescence microscopy and flow cytometry. β-catenin promoter activity was checked by luciferase assay. Results: We observed reduced EMT in ovarian cancer cells upon co-activation with TGFβ1 and LiCl as shown by the expressions of epithelial/mesenchymal markers and the EMT promoting factor, Snail1, accompanied by decrease in the invasion and migration of the cells compared to individual pathway activation. A detailed study of the mechanism suggested reduction in the β-catenin and p-GSK3b (Ser 9) levels to be the driving cause of this phenomenon, which was reversed upon co-activation with higher concentrations of LiCl. Conclusions: Therefore, tumourigenesis might be affected by the concentration of ligand/ growth factors for the respective signalling pathways activated in the tumour microenvironment and interaction between them might alter tumourigenesis.

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