Ghrelin attenuates the growth of HO-8910 ovarian cancer cells through the ERK pathway

Ovarian cancer is one of the most common causes of death from gynecologic tumors and is an important public health issue. Ghrelin is a recently discovered bioactive peptide that acts as a natural endogenous ligand of the growth hormone secretagogue receptor (GHSR). Several studies have identified th...

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Main Authors: Bai, R.X., Wang, W.P., Zhao, P.W., Li, C.B.
Format: Online
Language:English
Published: Associação Brasileira de Divulgação Científica 2016
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4763821/
id pubmed-4763821
recordtype oai_dc
spelling pubmed-47638212016-03-07 Ghrelin attenuates the growth of HO-8910 ovarian cancer cells through the ERK pathway Bai, R.X. Wang, W.P. Zhao, P.W. Li, C.B. Biomedical Sciences Ovarian cancer is one of the most common causes of death from gynecologic tumors and is an important public health issue. Ghrelin is a recently discovered bioactive peptide that acts as a natural endogenous ligand of the growth hormone secretagogue receptor (GHSR). Several studies have identified the protective effects of ghrelin on the mammalian reproductive system. However, little research has been done on the effects of ghrelin on ovarian cancer cells, and the underlying mechanisms of these effects. We sought to understand the potential involvement of mitogen-activated protein kinases (MAPKs) in ghrelin-mediated inhibition of growth of the ovarian line HO-8910. We applied different concentrations of ghrelin and an inhibitor of the ghrelin receptor (D-Lys3-GHRP-6) to HO-8910 cells and observed the growth rate of cells and changes in phosphorylation of the MAPKs ERK1/2, JNK and p38. We discovered that ghrelin-induced apoptosis of HO-8910 cells was though phosphorylated ERK1/2, and that this phosphorylation (as well as p90rsk phosphorylation) was mediated by the GHSR. The ERK1/2 pathway is known to play an essential part in the ghrelin-mediated apoptosis of HO-8910 cells. Hence, our study suggests that ghrelin inhibits the growth of HO-8910 cells primarily through the GHSR/ERK pathway. Associação Brasileira de Divulgação Científica 2016-02-02 /pmc/articles/PMC4763821/ /pubmed/26840702 http://dx.doi.org/10.1590/1414-431X20155043 Text en http://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Bai, R.X.
Wang, W.P.
Zhao, P.W.
Li, C.B.
spellingShingle Bai, R.X.
Wang, W.P.
Zhao, P.W.
Li, C.B.
Ghrelin attenuates the growth of HO-8910 ovarian cancer cells through the ERK pathway
author_facet Bai, R.X.
Wang, W.P.
Zhao, P.W.
Li, C.B.
author_sort Bai, R.X.
title Ghrelin attenuates the growth of HO-8910 ovarian cancer cells through the ERK pathway
title_short Ghrelin attenuates the growth of HO-8910 ovarian cancer cells through the ERK pathway
title_full Ghrelin attenuates the growth of HO-8910 ovarian cancer cells through the ERK pathway
title_fullStr Ghrelin attenuates the growth of HO-8910 ovarian cancer cells through the ERK pathway
title_full_unstemmed Ghrelin attenuates the growth of HO-8910 ovarian cancer cells through the ERK pathway
title_sort ghrelin attenuates the growth of ho-8910 ovarian cancer cells through the erk pathway
description Ovarian cancer is one of the most common causes of death from gynecologic tumors and is an important public health issue. Ghrelin is a recently discovered bioactive peptide that acts as a natural endogenous ligand of the growth hormone secretagogue receptor (GHSR). Several studies have identified the protective effects of ghrelin on the mammalian reproductive system. However, little research has been done on the effects of ghrelin on ovarian cancer cells, and the underlying mechanisms of these effects. We sought to understand the potential involvement of mitogen-activated protein kinases (MAPKs) in ghrelin-mediated inhibition of growth of the ovarian line HO-8910. We applied different concentrations of ghrelin and an inhibitor of the ghrelin receptor (D-Lys3-GHRP-6) to HO-8910 cells and observed the growth rate of cells and changes in phosphorylation of the MAPKs ERK1/2, JNK and p38. We discovered that ghrelin-induced apoptosis of HO-8910 cells was though phosphorylated ERK1/2, and that this phosphorylation (as well as p90rsk phosphorylation) was mediated by the GHSR. The ERK1/2 pathway is known to play an essential part in the ghrelin-mediated apoptosis of HO-8910 cells. Hence, our study suggests that ghrelin inhibits the growth of HO-8910 cells primarily through the GHSR/ERK pathway.
publisher Associação Brasileira de Divulgação Científica
publishDate 2016
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4763821/
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