Long non‑coding RNA SNHG3 promotes prostate cancer progression by sponging microRNA‑1827
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- Published online on: June 27, 2022 https://doi.org/10.3892/ol.2022.13401
- Article Number: 281
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Copyright: © Hu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
Long non‑coding RNAs (lncRNAs) are important biological factors that contribute to the initiation and progression of different types of cancer, including gastric, bladder and colorectal cancer. Small nucleolar RNA host gene 3 (SNHG3) has been implicated in prostate cancer (PCa) progression. However, the expression pattern and function of SNHG3 in PCa remain unclear, impeding the development of novel treatment strategies for this cancer. The present study aimed to investigate a combination of molecular and biochemical approaches to determine the role of SNHG3 in patients at different stages of disease, and elucidate the pathway by which SNHG3 affects PCa progression. A Cell Counting Kit‑8 assay was used to assess cell proliferation. Transwell assays were used to analyze cell migration and invasion. Reverse transcription‑quantitative PCR and western blotting were used to evaluate the expression levels of RNAs and proteins, respectively. The results demonstrated that SNHG3 expression was upregulated in PCa tissues downloaded from The Cancer Genome Atlas database, which was associated with poor prognosis. Furthermore, cell proliferation, migration and invasion were significantly inhibited following SNHG3 knockdown in vitro, the effects of which were reversed following overexpression of SNHG3 in PCa cells. Bioinformatic analysis revealed that microRNA (miRNA/miR)‑1827 was a downstream target of SNHG3. The direct interaction between SNHG3 and miR‑1827 was validated via the dual‑luciferase reporter and RNA immunoprecipitation assays. Pearson's correlation analysis demonstrated that SNHG3 expression was negatively correlated with miR‑1827 expression at different stages of PCa. Furthermore, rescue assays indicated that cotransfection with small interfering‑SNHG3 and miR‑1827 inhibitor reversed the effects of SNHG3 knockdown on cell proliferation, migration and invasion. In addition, SNHG3 knockdown in vivo suppressed tumor growth. Notably, lncRNA SNHG3 promoted PCa progression through miR‑1827 via the Wnt/AKT/mTOR pathway. Taken together, the results of the present study suggest that SNHG3 promotes PCa progression by sponging miR‑1827, indicating that SNHG3 may be a promising diagnostic and therapeutic target of PCa.
