Background: Androgen receptor (AR) and long non-coding RNAs (lncRNA) play important roles in the initiation and progression of prostate cancer (PCa). The present study was designed to investigate whether lncRNA growth arrest-specific 5 (GAS5) is involved in the regulation of dexamethasone on the proliferation of AR+ PCa and AR- PCa cell lines.
Methods: Cell proliferation and cell cycle distribution were assessed using MTT assay and flow cytometry, respectively. GAS5 expression was examined by quantitative real-time PCR. AR protein level was examined by Western blot. RNA immunoprecipitation and RNA pull-down were performed to analyze the binding of GAS5 to AR.
Results: In AR- PCa cell line PC3, dexamethasone upregulated GAS5 expression, induced cell cycle arrest in the G0/G1 phase and inhibited cell proliferation, which were enhanced by GAS5 overexpression and attenuated by GAS5 silencing. However, in AR+ PCa cell line 22Rv1, dexamethasone had no obvious effects on GAS5 expression, cell cycle distribution and cell proliferation. AR was localized in the cytoplasm and bound to GAS5, counteracting the proliferation-inhibitory effect of GAS5.
Conclusion: Taken together, GAS5 participates in the regulation of dexamethasone on the proliferation of AR+ PCa and AR- PCa cell lines.
Keywords: Androgen receptor; Dexamethasone; Growth arrest-specific 5; Proliferation; Prostate cancer.
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