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Endocrine Abstracts (2012) 29 P849

ICEECE2012 Poster Presentations Endocrine tumours and neoplasia (112 abstracts)

Gene expression profile of LNCaP human prostate cancer cells after treatment with an antagonist of growth hormone-releasing hormone

Z. Rekasi 1 , T. Czompoly 2 , M. Zarandi 3, & A. Schally 4


Veterans Affairs Medical Center and South Florida VA Foundation for Research and Education, Miami, FL, USA.


Antagonists of growth hormone-releasing hormone (GHRH-ant) may exert their antiproliferative effects directly on cancer cells, which are mediated by the tumoral GHRH receptors identified by us. Furthermore we showed that GHRH-ant are able to induce apoptosis in LNCaP human prostate cancer cells through a Ca2+-dependent pathway. However, the molecular features involved in the antiproliferative effect of GHRH-ant have not yet been elucidated. To study this, gene expression profile of LNCaP cancer cells treated with a GHRH-ant MZ-J-138 (10 μM) for 1, 5 or 18 hours was analyzed and compared to that of untreated control LNCaP cells. The genome-wide cDNA microarray chip type in the experiment was Illumina Human HT-12 v.4 Expression BeadChip. Expression profiling showed 181, 152, 16 up-regulated genes and 98, 43, 8 down-regulated genes in LNCaP cells treated with GHRH-ant for 1, 5, 18 hours, respectively (average fold difference >1.5; P<0.0001). We observed overexpression of PMEPA1, BRCA1, KLF6, FANCG, RBL1, E2F2 and down-regulation of SLC45A3, TMPRSS2, MYC in LNCaP cells after treatment with GHRH-ant. In addition, many cell cycle genes are constituently activated in treated LNCaP cells. The up-regulated negative regulators of cell proliferation and the down-regulation of some factors expressed in high concentration in prostate cancer cells may explain why GHRH-ant can reduce cell proliferation of LNCaP cells. Our data suggest also the involvement of p53-dependent and independent mechanisms in the antiproliferative effect of GHRH-ant. Treatment with GHRH-ant may offer a new approach to the therapy of prostate and other hormone-sensitive cancers (supported by OTKA K 068452).

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details unavailable.

Volume 29

15th International & 14th European Congress of Endocrinology

European Society of Endocrinology 

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