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Long non-coding RNA GAS5 regulates apoptosis in prostate cancer cell lines.
M R Pickard1, M Mourtada-Maarabouni, G T Williams
1School of Life Sciences, Keele University, Keele, UK. m.r.pickard@keele.ac.uk
Biochimica Et Biophysica Acta
|May 17, 2013
Summary
Growth Arrest-Specific 5 (GAS5) long non-coding RNA (lncRNA) promotes prostate cancer cell death. Lower GAS5 levels may decrease chemotherapy effectiveness, highlighting its role in prostate cancer survival.
Area of Science:
- Molecular Biology
- Cancer Research
- RNA Biology
Background:
- Small non-coding RNAs' role in apoptosis is known, but long non-coding RNAs (lncRNAs) are less studied.
- Growth Arrest-Specific 5 (GAS5) encodes snoRNAs and produces a lncRNA that represses glucocorticoid receptors.
- GAS5 negatively impacts lymphoid and breast cell survival and is altered in various cancers.
Purpose of the Study:
- To investigate the role of GAS5 in prostate cancer cell survival.
- To determine if GAS5 influences prostate cancer cell apoptosis and response to therapy.
Main Methods:
- Prostate cancer cell lines (22Rv1, PC-3) were transfected with GAS5 plasmids or siRNAs.
- Cell survival and apoptosis were assessed after GAS5 manipulation.
- The effect of GAS5 on UV-C irradiation and chemotherapy-induced cell death was evaluated.
Main Results:
- GAS5 overexpression increased apoptosis and decreased survival in prostate cancer cells.
- GAS5 knockdown attenuated UV-C irradiation and chemotherapy-induced cell death.
- Cell death strongly correlated with cellular GAS5 levels.
Conclusions:
- GAS5 promotes prostate cancer cell apoptosis, with the lncRNA being sufficient for this activity.
- Low GAS5 expression may reduce the efficacy of chemotherapeutic agents in prostate cancer.
- GAS5 is identified as the first death-promoting lncRNA in prostate cells.
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