IDO promotes the proliferation and invasion of prostate cancer cells through KYNU

• Published in: Genes & genomics Vol. 45; no. 3; pp. 367 - 376
• Main Authors: Zhou, Hongqing, Wang, Wei, Liu, Mingsheng, Xie, Pingbo, Deng, Tibin, Peng, Jiaxi, Xu, Chenxiang
• Format: Journal Article
• Language: English
• Published: Singapore Springer Nature Singapore 01.03.2023; Springer; Springer Nature B.V; 한국유전학회
• Subjects: Analysis; Animal Genetics and Genomics; Apoptosis; Biomedical and Life Sciences; Cell culture; Cell Line, Tumor; Cell Proliferation; Cholecystokinin; Dioxygenase; Flow cytometry; Human Genetics; Humans; Life Sciences; Male; Medical prognosis; Microbial Genetics and Genomics; Plant Genetics and Genomics; Prognosis; Prostate cancer; Prostatic Neoplasms - pathology; Proteins; Research Article; 생물학; Proliferation; Indoleamine-2, 3-dioxygenase; Prostate cancer; KYNU; Invasion
• ISSN: 1976-9571; 2092-9293
• DOI: 10.1007/s13258-022-01316-y

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.