The inhibition effect of psoralen on prostate cancer PC3 cells via down-regulation of long non-coding RNA
Shushang Chen1,2, Mingfang Weng2, Ronghui Lin1
1Department of Urology, Clinical Oncology School of Fujian Medical University, Fujian Cancer Hospital, Fuzhou, China.
Background:
New medications are needed to improve outcomes of castration-resistant prostate cancer (CRPC). Psoralen has been reported to have anti-cancer properties for various tumors, but there are limited reports about psoralen treatment in prostate cancer (PCa). This study aimed to investigate the effect of psoralen on PC3 cells and to investigate potential underlying mechanisms of action.
Methods:
The effect of psoralen on the proliferation and cell cycle progression of PC3 cells was determined using Cell Counting Kit-8 (CCK-8) test and flow cytometry, respectively. The differential gene profiles in PC3 cells treated with psoralen were determined with microarray analyses. The effect of psoralen on long non-coding RNA (lncRNA) ENST00000510619 expression in PC3 cells was detected by real-time quantitative polymerase chain reaction (RT-qPCR). The effect of psoralen and transfection of small interfering lnc-RNA (si-lncRNA) ENST00000510619 on cell viability, invasion ability, and migratory activity of PC3 cells were evaluated using the CCK-8 test, transwell assay, and wound healing, respectively.
Results:
Psoralen significantly inhibited PC3 cells in a concentration- and time-dependent manner and caused G1 phase and G2/M phase cycle arrests. When screened with a fold change (FC) of ≥2 and a P value of <0.05, 1,716 lncRNAs and 1,160 messenger RNAs (mRNAs) were significantly up-regulated, whereas 3,269 lncRNAs and 3,263 mRNAs were significantly down-regulated in PC3 cells after psoralen treatment. Among the differentially down-regulated lncRNAs in which the signal of the probe showed significant differences compared to the background, lncRNA ENST00000510619 had the highest FC. The expression of lncRNA ENST00000510619 was shown to be down-regulated by psoralen in a concentration-dependent manner. CCK-8 assay, wound healing, and transwell assay showed that both psoralen and si-lncRNA ENST00000510619 transfection significantly inhibited the activity, invasion, and migration of PC3 cells (P<0.01 for all).
Conclusions:
Psoralen was confirmed to inhibit proliferation and block the cell cycle in PC3 cells in this in vitro study. The molecular mechanism involves multiple differentially expressed lncRNAs and mRNAs and is related to the down-regulation of lncRNA ENST000000510619 expression. This study provides the experimental basis for the development of psoralen as a novel anti-CRPC drug and for the consideration of lncRNA ENST00000510619 as a potential clinical target for CRPC.
Insights
Psoralen inhibits castration-resistant prostate cancer (CRPC) cell growth by arresting the cell cycle and down-regulating lncRNA ENST00000510619. This suggests psoralen
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Castration-resistant prostate cancer (CRPC) requires novel therapeutic agents.
- Psoralen exhibits anti-cancer properties, but its role in prostate cancer (PCa) is underexplored.
- This study investigates psoralen's effects on PC3 prostate cancer cells.
Purpose of the Study:
- To evaluate the anti-cancer effects of psoralen on PC3 cells.
- To elucidate the underlying molecular mechanisms, including gene expression changes and long non-coding RNA (lncRNA) involvement.
- To assess the potential of psoralen and lncRNA ENST00000510619 as therapeutic targets for CRPC.
Main Methods:
- Cell proliferation assessed by Cell Counting Kit-8 (CCK-8) assay.
- Cell cycle progression analyzed via flow cytometry.
- Differential gene expression profiles determined using microarray analysis.
- lncRNA ENST00000510619 expression quantified by RT-qPCR.
- Cell viability, invasion, and migration evaluated after psoralen or si-lncRNA ENST00000510619 treatment.
Main Results:
- Psoralen significantly inhibited PC3 cell proliferation in a dose- and time-dependent manner.
- Psoralen induced G1 and G2/M phase cell cycle arrest.
- Microarray analysis revealed significant differential expression of numerous lncRNAs and mRNAs.
- Psoralen down-regulated lncRNA ENST00000510619 expression.
- Both psoralen and si-lncRNA ENST00000510619 inhibited PC3 cell viability, invasion, and migration.
Conclusions:
- Psoralen effectively inhibits PC3 cell proliferation and induces cell cycle arrest in vitro.
- The anti-cancer mechanism involves modulation of multiple lncRNAs and mRNAs, notably the down-regulation of lncRNA ENST00000510619.
- Psoralen shows promise as a novel anti-CRPC therapeutic, with lncRNA ENST00000510619 as a potential clinical target.
Related Concept Videos
MicroRNAs
lncRNA - Long Non-coding RNAs
Abnormal Proliferation
Experimental RNAi


