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Updated: Jul 26, 2025
miRNA Expression Analyses in Prostate Cancer Clinical Tissues
Published on: September 8, 2015
Analyzing roles of small nucleolar RNA host gene 25 from clinical, molecular target and tumor formation in prostate
Zelin Liu1, Shuai Ke2, Qinghua Wang2
1Department of Urology, Renmin Hospital of Wuhan University, Wuhan, 430060, China; Britton Chance Center for Biomedical Photonics, Wuhan National Laboratory for Optoelectronics, Huazhong University of Science and Technology, Wuhan, 430074, China.
Background:
Prostate cancer (PCa) is one of the most deadly and metastatic cancers of the urinary tract. Latest studies have confirmed that long non-coding RNAs (lncRNAs) play a crucial role in a variety of cancers. Some of these lncRNAs code for small nucleolar RNAs (snoRNAs), called small nucleolar RNA host genes (SNHGs), which exert some value in predicting the prognosis of certain cancer patients, but little is known regarding the function of SNHGs within the PCa.
Aim Of The Study:
To explore the expression distribution and differential analysis of SNHGs in different tumors using RNA-seq and survival data from TCGA and GTEx, and to assess the potential impacts of the lncRNA SNHG25 on human PCa. To validate the expression of SNHG25 using experimental data and to investigate in detail its particular molecular biological function on PCa both in vivo and in vitro.
Methods:
LncRNA SNHG25 expression was analyzed by bioinformatic prediction and qPCR. CCK-8, EdU, transwell, wound healing, and western blotting assays were conducted to investigate the main role of lncRNA SNHG25 in PCa. Xenograft tumour growth model in nude mice was surveyed by in vivo imaging and Ki-67 staining. AKT pathway activator (SC79) was used to verify the interaction among SNHG25 and PI3K/AKT signaling pathway.
Results:
Bioinformatics analysis and experimental research illuminated that the expression of lncRNA SNHG25 was observably up-regulated in PCa tissues and cells. Moreover, SNHG25 knockdown restrained PCa cell proliferation, invasion and migration, while promoting apoptosis. Xenografts model confirmed that the si-SNHG25 group had a significant inhibitory effect on PCa tumour growth in vivo. Additionally, a series of gain-of-function analyses suggested that SNHG25 could activate the PI3K/AKT pathway to accelerate PCa progression.
Conclusions:
These in vitro and in vivo findings demonstrate that SNHG25 is highly expressed in PCa and facilitates PCa development through regulation of PI3K/AKT signaling pathway. SNHG25 acts as an oncogene to predict tumour malignancy and survival in PCa patients and may therefore become a promising potential molecular target for early detection and therapy of lethal PCa.
Insights
This study reveals that the long non-coding RNA SNHG25 is highly expressed in prostate cancer (PCa), promoting tumor growth and progression by activating the PI3K/AKT pathway. SNHG25 shows potential as a biomarker for PCa malignancy and survival.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Prostate cancer (PCa) is a deadly urinary tract malignancy.
- Long non-coding RNAs (lncRNAs), including small nucleolar RNA host genes (SNHGs), are implicated in various cancers.
- The specific role of SNHGs in PCa remains largely unknown.
Purpose of the Study:
- To investigate the expression and function of SNHGs in PCa.
- To analyze the impact of lncRNA SNHG25 on PCa development.
- To validate SNHG25's role in vitro and in vivo, focusing on the PI3K/AKT pathway.
Main Methods:
- Bioinformatic analysis of TCGA and GTEx data for SNHG expression.
- Quantitative PCR (qPCR) for SNHG25 validation.
- Cellular assays (CCK-8, EdU, Transwell, wound healing) and Western blotting.
- In vivo xenograft models and Ki-67 staining.
- PI3K/AKT pathway activation studies using SC79.
Main Results:
- SNHG25 was significantly upregulated in PCa tissues and cells.
- Knockdown of SNHG25 inhibited PCa cell proliferation, invasion, and migration, while promoting apoptosis.
- In vivo studies showed SNHG25 knockdown significantly suppressed tumor growth.
- SNHG25 was found to activate the PI3K/AKT pathway, promoting PCa progression.
Conclusions:
- SNHG25 is highly expressed in PCa and drives tumor development via the PI3K/AKT pathway.
- SNHG25 functions as an oncogene in PCa.
- SNHG25 holds promise as a molecular target for PCa detection and therapy.
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