Antagonist of Growth Hormone-Releasing Hormone Receptor MIA-690 Suppresses the Growth of Androgen-Independent Prostate Cancers.
Male
Humans
Animals
Mice
Mice, Nude
Cell Line, Tumor
Gefitinib
/ pharmacology
Receptors, Pituitary Hormone-Regulating Hormone
/ metabolism
Receptors, Neuropeptide
/ metabolism
Xenograft Model Antitumor Assays
Cell Proliferation
/ drug effects
Prostatic Neoplasms, Castration-Resistant
/ drug therapy
Cell Survival
/ drug effects
ErbB Receptors
/ metabolism
PC-3 Cells
Growth Hormone-Releasing Hormone
/ antagonists & inhibitors
Prostatic Neoplasms
/ metabolism
Pyrrolidines
/ pharmacology
Drug Synergism
Cell Adhesion
/ drug effects
Pyrroles
/ pharmacology
Sermorelin
/ analogs & derivatives
EGFR inhibitor
GHRH-R antagonist
combination therapy
prostate cancer
transactivation
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
18 Oct 2024
18 Oct 2024
Historique:
received:
24
08
2024
revised:
08
10
2024
accepted:
14
10
2024
medline:
26
10
2024
pubmed:
26
10
2024
entrez:
26
10
2024
Statut:
epublish
Résumé
The development of resistance remains the primary challenge in treating castration-resistant prostate cancer (CRPC). GHRH receptors (GHRH-R), which are coupled to G-proteins (GPCRs), can mediate EGFR transactivation, offering an alternative pathway for tumour survival. This study aimed to evaluate the effects of the GHRH-R antagonist MIA-690, in combination with the EGFR inhibitor Gefitinib, on cell viability, adhesion, gelatinolytic activity, and the cell cycle in advanced prostate cancer PC-3 cells. The findings demonstrate a synergistic effect between MIA-690 and Gefitinib, leading to the inhibition of cell viability, adhesion, and metalloprotease activity. Cell cycle analysis suggests that both compounds induce cell cycle arrest, both individually and in combination. Furthermore, similar effects of the GHRH-R antagonist MIA-690 combined with Gefitinib were observed in PC-3 tumours developed by subcutaneous injection in athymic nude mice 36 days post-inoculation. These results indicate that combined therapy with a GHRH-R antagonist and an EGFR inhibitor exerts a stronger antitumor effect compared to monotherapy by preventing transactivation between EGFR and GHRH-R in CRPC.
Identifiants
pubmed: 39456984
pii: ijms252011200
doi: 10.3390/ijms252011200
pii:
doi:
Substances chimiques
Gefitinib
S65743JHBS
Receptors, Pituitary Hormone-Regulating Hormone
0
Receptors, Neuropeptide
0
somatotropin releasing hormone receptor
F8L0ODC9D7
ErbB Receptors
EC 2.7.10.1
GHRH(1-29)NH2, (PhAc-Ada)(0)-Tyr(1), Arg(2), Fpa(5,6), Ala(8), Har(9), Tyr(Me)(10), His(11), Orn(12,) Abu(15), His(20), Orn(21), Nle(27), Arg(28), Har(29)-
0
Growth Hormone-Releasing Hormone
9034-39-3
Pyrrolidines
0
Pyrroles
0
Sermorelin
86168-78-7
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Instituto de Salud Carlos III
ID : P118/00526