The long non-coding RNA, GHSROS, mediates prostate cancer growth

Paper


Thomas, Patrick, Walpole, Carina Maree, Jeffery, Penny, Jovanovic, Lidija, Herington, Adrian, Nelson, Colleen, Whiteside, Eliza, Veedu, Rakesh, Seim, Inge and Chopin, Lisa. 2018. "The long non-coding RNA, GHSROS, mediates prostate cancer growth ." Annual Scientific Meeting of the Endocrine Society of Australia 2016. Gold Coast, Australia 21 - 24 Aug 2016 United Kingdom . John Wiley & Sons. https://doi.org/10.1111/cen.13259
Paper/Presentation Title

The long non-coding RNA, GHSROS, mediates prostate cancer growth

Presentation TypePaper
AuthorsThomas, Patrick, Walpole, Carina Maree, Jeffery, Penny, Jovanovic, Lidija, Herington, Adrian, Nelson, Colleen, Whiteside, Eliza, Veedu, Rakesh, Seim, Inge and Chopin, Lisa
Journal or Proceedings TitleClinical Endocrinology
Journal Citation89 (S1), pp. 24-24
Number of Pages1
YearJun 2018
PublisherJohn Wiley & Sons
Place of PublicationUnited Kingdom
ISSN0300-0664
1365-2265
Digital Object Identifier (DOI)https://doi.org/10.1111/cen.13259
Web Address (URL) of Paperhttps://onlinelibrary.wiley.com/doi/10.1111/cen.13259
Web Address (URL) of Conference Proceedingshttps://onlinelibrary.wiley.com/toc/13652265/2017/86/S1
Conference/EventAnnual Scientific Meeting of the Endocrine Society of Australia 2016
Event Details
Annual Scientific Meeting of the Endocrine Society of Australia 2016
Delivery
In person
Event Date
21 to end of 24 Aug 2016
Event Location
Gold Coast, Australia
Abstract

Long non-coding RNAs (lncRNAs) play key regulatory roles in cancer progression and are novel therapeutic targets1. We have discovered a lncRNA on the antisense strand of the ghrelin receptor gene (GHSR), termed GHSROS (GHSR opposite strand). Using quantitative RT-PCR we demonstrated that GHSROS is highly expressed in a subset of high grade prostate cancers. GHSROS over-expression significantly increased cell proliferation in the PC3 (1.76 ± 0.18 fold, P < 0.01) and DU145 prostate cancer cell lines compared to vector control (1.74 fold ± 0.73 P < 0.01), using xCELLigence real time cell analysis. GHSROS also increased cell migration in these cell lines compared to vector control (1.54 ± 0.35 fold in the PC3 cell line, P < 0.05, and 1.94 ± 0.43 fold in the DU145 cell line, P < 0.01). RNA sequencing in the PC3-GHSROS cell line demonstrated that genes associated with a metastatic prostate cancer gene signature were suppressed or induced by GHSROS. Using novel locked nucleic acid antisense oligonucleotides designed to target GHSROS, GHSROS silencing inhibited cell proliferation (−1.14 ± 0.07 fold, P < 0.05) and migration (−1.9 ± 0.14 fold, P < 0.05) in the PC3 cell line. Tumour growth was investigated in vivo using a subcutaneous NOD/SCID mouse xenograft model. Tumour volume was significantly increased in the PC3 and DU145 cell line xenografts over-expressing GHSROS (P < 0.05). GHSROS may have clinical significance in prostate cancer as it is highly expressed in a significant subset of prostate cancers and is associated with a metastatic gene signature. GHSROS plays a role in cell proliferation, migration and tumour growth and may provide a useful target for the development of novel antisense therapies for prostate cancer treatment.

Contains Sensitive ContentDoes not contain sensitive content
ANZSRC Field of Research 2020321109. Predictive and prognostic markers
321101. Cancer cell biology
321108. Molecular targets
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Byline AffiliationsQueensland University of Technology
Princess Alexandra Hospital, Australia
Centre for Health Research
University of Southern Queensland
Murdoch University
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