GHRH antagonist inhibits focal adhesion kinase (FAK) and decreases expression of vascular endothelial growth factor (VEGF) in human lung cancer cells in vitro

Agnieszka Siejka, Nektarios Barabutis, Andrew V Schally

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Lung cancers which show increased vascularization and high microvessel density are considered highly metastatic and with poor prognosis. Growth hormone releasing hormone (GHRH) antagonists are anticancer agents without adverse events in lung cancer tumor models. In the present study we investigated the in vitro effect of GHRH antagonist, MZ-5-156, on focal adhesion kinase (FAK) activity, on the expression of MMP-2 and MMP-9 metalloproteinases, as well as on vascular endothelial growth factor (VEGF) levels in A549 non-small cell lung (NSCLC) cancer cells and H727 bronchial carcinoid cells. We demonstrate for the first time that GHRH antagonist, MZ-5-156, inhibits FAK signaling in lung cancer cells and decreases the expression of additional factors involved in angiogenesis and invasion. In contrast, GHRH itself counteracted these effects. Our study contributes to the further understanding of the processes which govern the mechanism of action of GHRH and its antagonists in cancers.

Original languageEnglish
Pages (from-to)63-68
Number of pages6
JournalPeptides
Volume37
Issue number1
DOIs
StatePublished - Sep 1 2012

Fingerprint

Hormone Antagonists
Growth Hormone-Releasing Hormone
Focal Adhesion Protein-Tyrosine Kinases
Vascular Endothelial Growth Factor A
Lung Neoplasms
Cells
Matrix Metalloproteinase 9
Carcinoid Tumor
Microvessels
Matrix Metalloproteinases
Non-Small Cell Lung Carcinoma
Antineoplastic Agents
Tumors
Neoplasms
In Vitro Techniques
human VEGFA protein

Keywords

  • Focal adhesion kinase
  • GHRH
  • GHRH antagonist
  • Growth factor
  • Lung cancer
  • Metalloproteinase

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology
  • Physiology
  • Cellular and Molecular Neuroscience

Cite this

GHRH antagonist inhibits focal adhesion kinase (FAK) and decreases expression of vascular endothelial growth factor (VEGF) in human lung cancer cells in vitro. / Siejka, Agnieszka; Barabutis, Nektarios; Schally, Andrew V.

In: Peptides, Vol. 37, No. 1, 01.09.2012, p. 63-68.

Research output: Contribution to journalArticle

@article{0b767ecf98524d5d8b398b65ca94417c,
title = "GHRH antagonist inhibits focal adhesion kinase (FAK) and decreases expression of vascular endothelial growth factor (VEGF) in human lung cancer cells in vitro",
abstract = "Lung cancers which show increased vascularization and high microvessel density are considered highly metastatic and with poor prognosis. Growth hormone releasing hormone (GHRH) antagonists are anticancer agents without adverse events in lung cancer tumor models. In the present study we investigated the in vitro effect of GHRH antagonist, MZ-5-156, on focal adhesion kinase (FAK) activity, on the expression of MMP-2 and MMP-9 metalloproteinases, as well as on vascular endothelial growth factor (VEGF) levels in A549 non-small cell lung (NSCLC) cancer cells and H727 bronchial carcinoid cells. We demonstrate for the first time that GHRH antagonist, MZ-5-156, inhibits FAK signaling in lung cancer cells and decreases the expression of additional factors involved in angiogenesis and invasion. In contrast, GHRH itself counteracted these effects. Our study contributes to the further understanding of the processes which govern the mechanism of action of GHRH and its antagonists in cancers.",
keywords = "Focal adhesion kinase, GHRH, GHRH antagonist, Growth factor, Lung cancer, Metalloproteinase",
author = "Agnieszka Siejka and Nektarios Barabutis and Schally, {Andrew V}",
year = "2012",
month = "9",
day = "1",
doi = "10.1016/j.peptides.2012.07.010",
language = "English",
volume = "37",
pages = "63--68",
journal = "Peptides",
issn = "0196-9781",
publisher = "Elsevier Inc.",
number = "1",

}

TY - JOUR

T1 - GHRH antagonist inhibits focal adhesion kinase (FAK) and decreases expression of vascular endothelial growth factor (VEGF) in human lung cancer cells in vitro

AU - Siejka, Agnieszka

AU - Barabutis, Nektarios

AU - Schally, Andrew V

PY - 2012/9/1

Y1 - 2012/9/1

N2 - Lung cancers which show increased vascularization and high microvessel density are considered highly metastatic and with poor prognosis. Growth hormone releasing hormone (GHRH) antagonists are anticancer agents without adverse events in lung cancer tumor models. In the present study we investigated the in vitro effect of GHRH antagonist, MZ-5-156, on focal adhesion kinase (FAK) activity, on the expression of MMP-2 and MMP-9 metalloproteinases, as well as on vascular endothelial growth factor (VEGF) levels in A549 non-small cell lung (NSCLC) cancer cells and H727 bronchial carcinoid cells. We demonstrate for the first time that GHRH antagonist, MZ-5-156, inhibits FAK signaling in lung cancer cells and decreases the expression of additional factors involved in angiogenesis and invasion. In contrast, GHRH itself counteracted these effects. Our study contributes to the further understanding of the processes which govern the mechanism of action of GHRH and its antagonists in cancers.

AB - Lung cancers which show increased vascularization and high microvessel density are considered highly metastatic and with poor prognosis. Growth hormone releasing hormone (GHRH) antagonists are anticancer agents without adverse events in lung cancer tumor models. In the present study we investigated the in vitro effect of GHRH antagonist, MZ-5-156, on focal adhesion kinase (FAK) activity, on the expression of MMP-2 and MMP-9 metalloproteinases, as well as on vascular endothelial growth factor (VEGF) levels in A549 non-small cell lung (NSCLC) cancer cells and H727 bronchial carcinoid cells. We demonstrate for the first time that GHRH antagonist, MZ-5-156, inhibits FAK signaling in lung cancer cells and decreases the expression of additional factors involved in angiogenesis and invasion. In contrast, GHRH itself counteracted these effects. Our study contributes to the further understanding of the processes which govern the mechanism of action of GHRH and its antagonists in cancers.

KW - Focal adhesion kinase

KW - GHRH

KW - GHRH antagonist

KW - Growth factor

KW - Lung cancer

KW - Metalloproteinase

UR - http://www.scopus.com/inward/record.url?scp=84865258841&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84865258841&partnerID=8YFLogxK

U2 - 10.1016/j.peptides.2012.07.010

DO - 10.1016/j.peptides.2012.07.010

M3 - Article

C2 - 22819774

AN - SCOPUS:84865258841

VL - 37

SP - 63

EP - 68

JO - Peptides

JF - Peptides

SN - 0196-9781

IS - 1

ER -