Hongqing Zhou1, Wei Wang1, Mingsheng Liu1, Pingbo Xie1, Tibin Deng1, Jiaxi Peng1, Chenxiang Xu2,3. 1. The second ward of urology, First People's Hospital of Qujing City, 655000, Qujing, Yunnan, China. 2. The second ward of urology, First People's Hospital of Qujing City, 655000, Qujing, Yunnan, China. xcx715501410@126.com. 3. , No.1 Garden Road, Qilin District, Qujing City655000, Qujing, China. xcx715501410@126.com.
Abstract
BACKGROUND: Prostate cancer (PCa) is one of the most common malignant tumors in male. OBJECTIVE: To explore the effect of indoleamine-2, 3-dioxygenase (IDO) on the proliferation and invasion of PCa cells and the potential mechanism. METHODS: PCa tissues and normal adjacent tissues were collected from 43 PCa patients. The expression of IDO in PCa tissues and cell lines were detected. The String website was used to search for IDO-related proteins. The GEPIA website was used to analyze the relationship between KYNU and the prognosis of PCa. Cells models of IDO overexpression and/or KYNU silencing were constructed to verify the role of KYNU in regulating PCa. The cell proliferation, apoptosis and invasion ability of PCa cells were detected by CCK-8 assay, Flow cytometry and Transwell assay. RESULTS: The IDO levels in PCa tissues and cells were higher than those in normal tissues and cells, which promoted the proliferation and invasion of LNCaP cells, and inhibited apoptosis. Silencing IDO inhibited the cells proliferation and invasion activities, and promoted the cell apoptosis. The high expression of KYNU was related to the poor disease free survival of PCa patients. Inhibiting KYUN significantly inhibited the promotion of PCa induced by IDO. CONCLUSION: IDO is overexpressed in PCa, which promotes the proliferation and invasion of PCa cells, and the cancer-promoting mechanism may be related to KYNU.
BACKGROUND: Prostate cancer (PCa) is one of the most common malignant tumors in male. OBJECTIVE: To explore the effect of indoleamine-2, 3-dioxygenase (IDO) on the proliferation and invasion of PCa cells and the potential mechanism. METHODS: PCa tissues and normal adjacent tissues were collected from 43 PCa patients. The expression of IDO in PCa tissues and cell lines were detected. The String website was used to search for IDO-related proteins. The GEPIA website was used to analyze the relationship between KYNU and the prognosis of PCa. Cells models of IDO overexpression and/or KYNU silencing were constructed to verify the role of KYNU in regulating PCa. The cell proliferation, apoptosis and invasion ability of PCa cells were detected by CCK-8 assay, Flow cytometry and Transwell assay. RESULTS: The IDO levels in PCa tissues and cells were higher than those in normal tissues and cells, which promoted the proliferation and invasion of LNCaP cells, and inhibited apoptosis. Silencing IDO inhibited the cells proliferation and invasion activities, and promoted the cell apoptosis. The high expression of KYNU was related to the poor disease free survival of PCa patients. Inhibiting KYUN significantly inhibited the promotion of PCa induced by IDO. CONCLUSION: IDO is overexpressed in PCa, which promotes the proliferation and invasion of PCa cells, and the cancer-promoting mechanism may be related to KYNU.