OBJECTIVE: Long noncoding RNAs (lncRNAs) act as an important role in many diseases. In this research, lncRNA PROX1-AS1 was explored to identify how it functioned in the development of prostate cancer (PC). PATIENTS AND METHODS: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was utilized to detect PROX1-AS1 expression in PC patients. Then, MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay, colony formation assay, and transwell assay were performed to identify its function in PC cells. Furthermore, the potential mechanism was also explored using mechanism assays. RESULTS: PROX1-AS1 expression level was significantly higher in PC tissue samples and cell lines. Results of MTT assay, colony formation assay, and transwell assay showed that cell proliferation and invasion were inhibited through the silence of PROX1-AS1 in PC cells, while cell proliferation and invasion were promoted through the overexpression of PROX1-AS1 in PC cells. Furthermore, the expression of miR-647 was upregulated via the silence of PROX1-AS1 in PC cells, while the expression of miR-647 was downregulated via the overexpression of PROX1-AS1 in PC cells. Further mechanism assays showed that miR-647 was a direct target of PROX1-AS1 in PC. Correlation analysis showed that miR-647 expression was negatively correlated with PROX1-AS1 expression in PC tissues. CONCLUSIONS: Results above suggested that PROX1-AS1 could enhance cell proliferation and invasion of PC cells by sponging miR-647 and might be applied as a novel target for the treatment of PC.
OBJECTIVE: Long noncoding RNAs (lncRNAs) act as an important role in many diseases. In this research, lncRNA PROX1-AS1 was explored to identify how it functioned in the development of prostate cancer (PC). PATIENTS AND METHODS: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was utilized to detect PROX1-AS1 expression in PCpatients. Then, MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay, colony formation assay, and transwell assay were performed to identify its function in PC cells. Furthermore, the potential mechanism was also explored using mechanism assays. RESULTS:PROX1-AS1 expression level was significantly higher in PC tissue samples and cell lines. Results of MTT assay, colony formation assay, and transwell assay showed that cell proliferation and invasion were inhibited through the silence of PROX1-AS1 in PC cells, while cell proliferation and invasion were promoted through the overexpression of PROX1-AS1 in PC cells. Furthermore, the expression of miR-647 was upregulated via the silence of PROX1-AS1 in PC cells, while the expression of miR-647 was downregulated via the overexpression of PROX1-AS1 in PC cells. Further mechanism assays showed that miR-647 was a direct target of PROX1-AS1 in PC. Correlation analysis showed that miR-647 expression was negatively correlated with PROX1-AS1 expression in PC tissues. CONCLUSIONS: Results above suggested that PROX1-AS1 could enhance cell proliferation and invasion of PC cells by sponging miR-647 and might be applied as a novel target for the treatment of PC.
Authors: Magdalena Rudzinska; Karolina H Czarnecka-Chrebelska; Ekaterina B Kuznetsova; Sofya V Maryanchik; Alessandro Parodi; Dmitry O Korolev; Nataliya Potoldykova; Yulia Svetikova; Andrey Z Vinarov; Marina V Nemtsova; Andrey A Zamyatnin Journal: Noncoding RNA Date: 2021-04-10