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Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
Published on: November 19, 2019
Long non-coding RNA PRRT3-AS1 silencing inhibits prostate cancer cell proliferation and promotes apoptosis and
Li Fan1, Hai Li1, Weihua Wang1
1Department of Urology, China and Japan Union Hospital of Jilin University, Changchun, 130033, P.R. China.
New Findings:
What is the central question of this study? What is the role of lncRNA PRRT3-AS1 in the regulation of peroxisome proliferator-activated receptor γ (PPARγ) gene-mediated mechanistic target of rapamycin (mTOR) signalling pathway in proliferation, apoptosis and autophagy of prostate cancer cells? What is the main finding and its importance? The targeting relation between lncRNA PRRT3-AS1 and PPARγ was verified, and it was demonstrated that silencing of lncRNA PRRT3-AS1 can upregulate apoptosis and autophagy yet downregulate proliferation, migration and invasion of prostate cancer cells through the mTOR signalling pathway. Further work is needed to consolidate the therapeutic value of lncRNA PRRT3-AS1 in clinical trials and treatment of prostate cancer.
Abstract:
Although long non-coding RNAs (lncRNAs) are correlated with multiple cancers, their molecular mechanisms in prostate cancer (PC) remain inadequately understood. This study investigated the effects of lncRNA PRRT3-AS1 on the progression of prostate cancer (PC) with involvement of peroxisome proliferator-activated receptor γ (PPARγ). Microarray analysis was used to identify the differentially expressed genes and lncRNAs associated with PC. RT-qPCR and western blot analysis were employed to test the expression of lncRNA PRRT3-AS1, mammalian target of rapamycin (mTOR) signalling pathway-, apoptosis- and autophagy-related genes. A scratch test, Transwell assay, CCK-8 assay, colony formation assay, flow cytometry and monodansylcadaverine staining were employed to identify the migration, invasion, proliferation activity, cell cycle and apoptosis and autophagy of PC3 cells, respectively. Tumorigenicity assays in nude mice were used to detect the tumorigenic ability. GSE55945 and GSE46602 datasets indicated that lncRNA PRRT3-AS1 was highly expressed in PC. PPARγ was predicted as a target gene of lncRNA PRRT3-AS1. Ectopic overexpression of PPARγ or lncRNA PRRT3-AS1 silencing led to inhibited cell viability, migration and invasion, and accelerated apoptosis. Furthermore, the delivery of si-PRRT3-AS1 or PPARγ vector to PC3 cells resulted in the regression of xenografts in nude mice. Based on the in vitro and in vivo experiments, silencing of lncRNA PRRT3-AS1 was observed to activate the PPARγ gene, which in turn could inhibit PC cell proliferation and promote apoptosis and autophagy by blocking the mTOR signalling pathway.
Insights
Silencing long non-coding RNA PRRT3-AS1 inhibits prostate cancer progression by activating PPARγ, which suppresses proliferation and enhances apoptosis and autophagy via the mTOR pathway. This finding offers potential therapeutic strategies for prostate cancer.
Area of Science:
- Molecular Biology
- Oncology
- Gene Regulation
Background:
- Long non-coding RNAs (lncRNAs) play roles in various cancers, but their specific functions in prostate cancer (PC) are not fully understood.
- Prostate cancer progression involves complex molecular mechanisms, including dysregulation of cell proliferation, apoptosis, and autophagy.
Purpose of the Study:
- To investigate the role of lncRNA PRRT3-AS1 in prostate cancer progression.
- To elucidate the regulatory relationship between lncRNA PRRT3-AS1, peroxisome proliferator-activated receptor γ (PPARγ), and the mechanistic target of rapamycin (mTOR) signaling pathway in prostate cancer cells.
Main Methods:
- Microarray analysis to identify differentially expressed genes and lncRNAs in PC.
- RT-qPCR and western blot to assess gene and protein expression.
- In vitro assays (scratch, Transwell, CCK-8, colony formation, flow cytometry, monodansylcadaverine staining) to evaluate cell proliferation, migration, invasion, apoptosis, and autophagy.
- In vivo tumorigenicity assays in nude mice.
Main Results:
- lncRNA PRRT3-AS1 was found to be highly expressed in prostate cancer tissues.
- Silencing lncRNA PRRT3-AS1 inhibited PC cell proliferation, migration, and invasion, while promoting apoptosis and autophagy.
- lncRNA PRRT3-AS1 silencing activated PPARγ, leading to the inhibition of the mTOR signaling pathway.
- Tumor growth was significantly reduced in mice treated with si-PRRT3-AS1 or PPARγ vector.
Conclusions:
- lncRNA PRRT3-AS1 promotes prostate cancer progression by targeting PPARγ and modulating the mTOR signaling pathway.
- Silencing lncRNA PRRT3-AS1 demonstrates therapeutic potential for prostate cancer by inhibiting tumor growth and enhancing apoptosis and autophagy.
- Further clinical investigations are warranted to validate lncRNA PRRT3-AS1 as a therapeutic target for prostate cancer.
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