The long non-coding RNA GHSROS reprograms prostate cancer cell lines toward a more aggressive phenotype

It is now appreciated that long non-coding RNAs (lncRNAs) are important players in orchestrating cancer progression. In this study we characterized , a human lncRNA gene on the opposite DNA strand (antisense) to the ghrelin receptor gene, in prostate cancer. The lncRNA was upregulated by prostate tu...

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Veröffentlicht in:PeerJ (San Francisco, CA) CA), 2021-02, Vol.9, p.e10280-e10280, Article e10280
Hauptverfasser: Thomas, Patrick B, Jeffery, Penny, Gahete, Manuel D, Whiteside, Eliza, Walpole, Carina, Maugham, Michelle, Jovanovic, Lidija, Gunter, Jennifer, Williams, Elizabeth, Nelson, Colleen, Herington, Adrian, Luque, Raul M, Veedu, Rakesh, Chopin, Lisa K, Seim, Inge
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Sprache:eng
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Zusammenfassung:It is now appreciated that long non-coding RNAs (lncRNAs) are important players in orchestrating cancer progression. In this study we characterized , a human lncRNA gene on the opposite DNA strand (antisense) to the ghrelin receptor gene, in prostate cancer. The lncRNA was upregulated by prostate tumors from different clinical datasets. Transcriptome data revealed that alters the expression of cancer-associated genes. Functional analyses in vitro showed that mediates tumor growth, migration and survival, and resistance to the cytotoxic drug docetaxel. Increased cellular proliferation of -overexpressing PC3, DU145, and LNCaP prostate cancer cell lines in vitro was recapitulated in a subcutaneous xenograft model. Conversely, in vitro antisense oligonucleotide inhibition of the lncRNA reciprocally regulated cell growth and migration, and gene expression. Notably, modulates the expression of , the loss of which may drive androgen receptor pathway-independent prostate tumor progression in a subset of prostate cancers. Collectively, our findings suggest that can reprogram prostate cancer cells toward a more aggressive phenotype and that this lncRNA may represent a potential therapeutic target.
ISSN:2167-8359
2167-8359
DOI:10.7717/peerj.10280