Open Access
hormone-releasing hormone (GHRH) antagonist on ovarian cancer cells through the EGFR-Akt pathway
Reads0
Chats0
TLDR
In this article, the effects of a new GHRH antagonist JMR-132, in ovarian cancer cell lines SKOV3 and CaOV3 expressing splice variant (SV)1 of gHRH receptors was examined by RT-PCR.Abstract:
Background: Antagonists of growth hormone-releasing hormone (GHRH) are being developed for the treatment of various human cancers. Methods: MTT assay was used to test the proliferation of SKOV3 and CaOV3. The splice variant expression of GHRH receptors was examined by RT-PCR. The expression of protein in signal pathway was examined by Western blotting. siRNA was used to block the effect of EGFR. Results: In this study, we investigated the effects of a new GHRH antagonist JMR-132, in ovarian cancer cell lines SKOV3 and CaOV3 expressing splice variant (SV)1 of GHRH receptors. MTT assay showed that JMR-132 had strong antiproliferative effects on SKOV3 and CaOV3 cells in both a time-dependent and dose-dependent fashion. JMR-132 also induced the activation and increased cleaved caspase3 in a time- and dose-dependent manner in both cell lines. In addition, JMR-132 treatments decreased significantly the epidermal growth factor receptor (EGFR) level and the phosphorylation of Akt (p-Akt), suggesting that JMR-132 inhibits the EGFR-Akt pathway in ovarian cancer cells. More importantly, treatment of SKOV3 and CaOV3 cells with 100 nM JMR-132 attenuated proliferation and the antiapoptotic effect induced by EGF in both cell lines. After the knockdown of the expression of EGFR by siRNA, the antiproliferative effect of JMR-132 was abolished in SKOV3 and CaOV3 cells. Conclusions: The present study demonstrates that the inhibitory effect of the GHRH antagonist JMR-132 on proliferation is due, in part, to an interference with the EGFR-Akt pathway in ovarian cancer cells.read more
Citations
More filters
Journal ArticleDOI
Ginsenoside Rg3 attenuates tumor angiogenesis via inhibiting bioactivities of endothelial progenitor cells
TL;DR: The xenograft tumor model clearly showed that Ginsenoside Rg3 suppresses tumor growth and tumor angiogenesis by inhibiting the mobilization of EPCs from the bone marrow microenvironment to the peripheral circulation and modulates VEGF-dependent tumorAngiogenesis.
Journal ArticleDOI
Growth hormone-releasing hormone receptor antagonists inhibit human gastric cancer through downregulation of PAK1-STAT3/NF-κB signaling.
Jinfeng Gan,Xiurong Ke,Jiali Jiang,Hongmei Dong,Zhimeng Yao,Yusheng Lin,Wan Lin,Xiao Wu,Shu-Mei Yan,Yixuan Zhuang,Wai Kit Chu,Renzhi Cai,Xianyang Zhang,Xianyang Zhang,Herman S. Cheung,Herman S. Cheung,Norman L. Block,Chi Pui Pang,Andrew V. Schally,Hao Zhang +19 more
TL;DR: It is reported that increased expression of growth hormone-releasing hormone receptor (GHRH-R) in tumor specimens is significantly associated with tumorigenic progression and poor clinical outcome of GC patients, and MIA-602 demonstrates excellent therapeutic potential against human GC.
Proceedings ArticleDOI
PAGE-Net: Interpretable and Integrative Deep Learning for Survival Analysis Using Histopathological Images and Genomic Data.
TL;DR: A biologically interpretable deep learning model (PAGE-Net) that integrates histopathological images and genomic data, not only to improve survival prediction, but also to identify genetic and Histopathological patterns that cause different survival rates in patients.
Journal ArticleDOI
Preclinical efficacy of growth hormone-releasing hormone antagonists for androgen-dependent and castration-resistant human prostate cancer
Cale D. Fahrenholtz,Ferenc G. Rick,Ferenc G. Rick,Maria I. Garcia,Marta Zarandi,Ren Zhi Cai,Norman L. Block,Norman L. Block,Andrew V. Schally,Andrew V. Schally,Kerry L. Burnstein +10 more
TL;DR: Evidence is provided of the preclinical efficacy of the GHRH antagonist MIA-602 for treatment of both androgen-dependent and CRPC for recurrent castration-resistant prostate cancer.
Journal ArticleDOI
Combination of GHRH antagonists and docetaxel shows experimental effectiveness for the treatment of triple-negative breast cancers
Stephan Seitz,Ferenc G. Rick,Andrew V. Schally,Andrea Treszl,F. Hohla,Luca Szalontay,Marta Zarandi,Olaf Ortmann,JB Engel,Stefan Buchholz +9 more
TL;DR: In this paper, the authors investigated the effectiveness of the treatment of MDA-MB-231 human triple-negative breast cancer (TNBC) with GHRH antagonist JMR-132 alone or in combination with docetaxel.
References
More filters
Journal ArticleDOI
MicroRNA-21 is an antiapoptotic factor in human glioblastoma cells.
TL;DR: It is shown that the highly malignant human brain tumor, glioblastoma, strongly over-expresses a specific miRNA, miR-21, which may contribute to the malignant phenotype by blocking expression of critical apoptosis-related genes.
Journal ArticleDOI
Epidermal growth factor receptors: critical mediators of multiple receptor pathways.
TL;DR: The receptor for epidermal growth factor was identified as a downstream element in different signaling pathways, expanding its classical function as a receptor for EGF-like ligands to a role as mediator of diverse signaling systems and as a switch point of a cellular communication network.
Reproductive Biology and Endocrinology
TL;DR: This review focuses on the basic biology of the satellite cell with emphasis on its role in muscle repair and parallels between embryonic myogenesis and muscle regeneration.
Journal ArticleDOI
Insulin-Like Growth Factor-I Protects Axotomized Rat Retinal Ganglion Cells from Secondary Death via PI3-K-Dependent Akt Phosphorylation and Inhibition of Caspase-3 In Vivo
TL;DR: Results indicate that intraocular application of IGF-I protects RGCs from death after ON transection in a dose-dependent manner and shows for the first time in vivothat IGF is neuroprotective via PI3-K-dependent Akt phosphorylation and by inhibition of caspase-3.