Aims
The incidence and detection rate of prostate cancer in China have been increasing in recent years. Radiotherapy is the ideal treatment for non-metastatic prostate cancer (PCa), but the effectiveness of radiotherapy is greatly discounted due to radio resistance. Therefore, relieving the radiotherapy resistance of PCa is key to improve the clinical efficacy of PCA. Main
Methods
Cell proliferation was estimated using the MTT and clone formation assays. Cell apoptosis was estimated using the Annexin V-FITC/propidium iodide (PI) staining assay. Glucose uptake and lactose and ATP production were used to detect glycolysis. Key findings: miR-223-3p was significantly upregulated in clinically collected urine samples and PCa cells with low radiosensitivity. Enhancing miR-223-3p reduced radiosensitivity further, while inhibiting miR-223-3p improved the radiosensitivity of PC3 and LNCaP cells. Importantly, miR-223-3p regulated radiosensitivity by enhancing cell glycolysis. FOXO3a was a key target of miRNA-223-3p regulating glycolysis and radiosensitivity. Overexpression of FOXO3a abated the glycolysis level and alleviated the radioresistance caused by enhancing miR-223-3p to a certain extent. Significance: This is novel research on the role of miR-223-3p in promoting radiotherapy resistance of PCa cells by activating glycolysis. This approach provides a new perspective and ideas for alleviating radiotherapy resistance of PCa cells.
Significance
This is novel research on the role of miR-223-3p in promoting radiotherapy resistance of PCa cells by activating glycolysis. This approach provides a new perspective and ideas for alleviating radiotherapy resistance of PCa cells.