Role of gonadotropin-releasing hormone of metastatic potential of ovarian cancer cells

2009 ◽  
Author(s):  
Wai-ting Cheung
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Metastatic Potential ◽  
Gonadotropin Releasing Hormone ◽  
Ovarian Cancer Cells ◽  
Releasing Hormone

scholarly journals Mechanism of gonadotropin-releasing hormone (GnRH)-I and -II-induced cell growth inhibition in ovarian cancer cells: role of the GnRH-I receptor and protein kinase C pathway

2006 ◽  
Vol 13 (1) ◽  
pp. 211-220 ◽  
Author(s):  
Ki-Yon Kim ◽  
Kyung-Chul Choi ◽  
Nelly Auersperg ◽  
Peter C K Leung
Keyword(s):  
Ovarian Cancer ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Gonadotropin Releasing Hormone ◽  
Ovarian Cancer Cells ◽  
Releasing Hormone ◽  
Proliferative Effect ◽  
Kinase C

In our previous studies, we demonstrated that ERK1/2 (extracellular signal-regulated protein kinase) and p38 MAPK (mitogen-activated protein kinase) are required for gonadotropin-releasing hormone (GnRH)-II-induced anti-proliferation of ovarian cancer cells. In the present study, we examined the role of the GnRH-I receptor, as well as the activation of protein kinase C (PKC), in the anti-proliferative effect induced by GnRH-I or II in ovarian cancer cells. Our results demonstrated that Antide, a GnRH-I antagonist, reversed the activation of ERK1/2 induced by GnRH-I or II and abolished the anti-proliferative effect of GnRH-I and II in ovarian cancer cells. Transfection of short-interfering RNA to abrogate the gene expression of the GnRH-I receptor reversed GnRH-I and II-induced anti-proliferation. These results indicate that GnRH-I or II induce anti-proliferation through the GnRH-I receptor in ovarian cancer cells. In addition, the activation of ERK1/2 by GnRH-I or II was mimicked by phorbol-12-myristate 13-acetate, a PKC activator. Pretreatment with GF109203X, an inhibitor of PKC, blocked GnRH-induced ERK1/2 activation and anti-proliferation. These results suggest that the activation of PKC is responsible for GnRH-induced ERK1/2 activation and anti-proliferation in ovarian cancer cells. Taken together, these results indicate that binding of GnRH-I and II to the GnRH-I receptor activates ERK1/2 through a PKC-dependent pathway and is essential for GnRH-induced anti-proliferation of ovarian cancer cells.

scholarly journals Effect of gonadotropin-releasing hormone agonist on ES-2 ovarian cancer cells

2014 ◽  
Vol 53 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Kuan-Hao Tsui ◽  
Wen-Ling Lee ◽  
Kok-Min Seow ◽  
Lin-Wei Yang ◽  
Shih-Yi Wang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Gonadotropin Releasing Hormone ◽  
Ovarian Cancer Cells ◽  
Releasing Hormone ◽  
Gonadotropin Releasing Hormone Agonist

scholarly journals Role of Gonadotropin-Releasing Hormone (GnRH) in Ovarian Cancer

Cells ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 437
Author(s):  
Carsten Gründker ◽  
Günter Emons
Keyword(s):  
Ovarian Cancer ◽  
Reproductive Organs ◽  
Gonadotropin Releasing Hormone ◽  
Regulation System ◽  
Ovarian Cancer Cells ◽  
Endocrine Regulation ◽  
Hpg Axis ◽  
Releasing Hormone ◽  
Gnrh Receptors

The hypothalamus–pituitary–gonadal (HPG) axis is the endocrine regulation system that controls the woman’s cycle. The gonadotropin-releasing hormone (GnRH) plays the central role. In addition to the gonadotrophic cells of the pituitary, GnRH receptors are expressed in other reproductive organs, such as the ovary and in tumors originating from the ovary. In ovarian cancer, GnRH is involved in the regulation of proliferation and metastasis. The effects on ovarian tumors can be indirect or direct. GnRH acts indirectly via the HPG axis and directly via GnRH receptors on the surface of ovarian cancer cells. In this systematic review, we will give an overview of the role of GnRH in ovarian cancer development, progression and therapy.

Sign in / Sign up

Export Citation Format

Share Document