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Long non-coding RNA lncHUPC1 induced by FOXA1 promotes tumor progression by inhibiting apoptosis via miR-133b/SDCCAG3 in prostate cancer.

ABSTRACT: Long non-coding RNAs (lncRNAs) were confirmed to be involved in regulating various malignant behaviors of tumor cells in prostate cancer (PCa). Using The Cancer Genome Atlas (TCGA) prostate adenocarcinoma datasets, several endogenous competing RNA (ceRNA) networks of lncRNA/miRNA/mRNA associated with the progression-free survival (PFS) and Gleason score (GS) were identified using bioinformatics analysis. lncRNA AC004447.2 (lncHUPC1, ENSG00000269131)/miR-133b/serologically defined colon cancer antigen-3 (SDCCAG3) was a newly identified ceRNA network that affected cell growth and apoptosis in PCa. Using q-PCR, lncHUPC1 and SDCCAG3 were found to be up-regulated in PCa cells, while miR-133b was down-regulated. The same results were found in tissue samples from 70 PCa cases. It was confirmed that the knockdown of lncHUPC1 increased the expression of miR-133b and decreased that of SDCCAG3, which further increased apoptosis and inhibited cell growth, while the miR-133b inhibitor partially reversed these effects. After transfection with miR-133b mimic after lncHUPC1-knockdown, the expression of miR-133b increased while that of SDCCAG3 reduced, and the apoptosis of the cells was more obvious and the growth of the cells was slower. Therefore, lncHUPC1 was confirmed to regulate SDCCAG3 by binding to miR-133b. Additionally, we found that the transcription factor Forkhead Box A1 (FOXA1) directly bound to the promoter of lncHUPC1 to activate it. In conclusion, the ceRNA network of lncHUPC1/miR-133b/SDCCAG3 affected the growth and apoptosis of PCa cells, and FOXA1 may be involved in the process as a transcription factor of lncHUPC1.

SUBMITTER: Liu M

PROVIDER: S-EPMC9251679 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description: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.

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Long non-coding RNA lncHUPC1 induced by FOXA1 promotes tumor progression by inhibiting apoptosis via miR-133b/SDCCAG3 in prostate cancer.

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