Circular RNA_LARP4 inhibits cell migration and invasion of prostate cancer by targeting FOXO3A

• Published in: European review for medical and pharmacological sciences Vol. 24; no. 10; p. 5303
• Main Authors: Weng, X-D, Yan, T, Liu, C-L
• Format: Journal Article
• Language: English
• Published: Italy 01.05.2020
• Subjects: Autoantigens - genetics; Autoantigens - metabolism; Cell Movement; Cell Proliferation; Cells, Cultured; Forkhead Box Protein O3 - genetics; Forkhead Box Protein O3 - metabolism; Humans; Male; Neoplasm Invasiveness; Prostatic Neoplasms - metabolism; Prostatic Neoplasms - pathology; Ribonucleoproteins - genetics; Ribonucleoproteins - metabolism; RNA, Circular - genetics; RNA, Circular - metabolism; SS-B Antigen
• DOI: 10.26355/eurrev_202005_21312

The importance of circular RNAs in malignant tumors causes more attention in researchers. Circular RNA_LARP4 is identified as a tumor suppressor in gastric cancer, but the role of circular RNA_LARP4 in prostate cancer (PCa) remains unclear. Our work aims to uncover whether and how circular RNA_LARP4 functions in the PCa development. Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was utilized to determine the level of circular RNA_LARP4 in PCa tissues and cell lines. The patients' prognosis was analyzed. Circular RNA_LARP4 lentivirus was constructed for transfection of PCa cells. Cell migrated and invaded ability was detected through wound healing assay and transwell assay. Western blot assay was performed to analyze the protein level of FOXO3A. The low circular RNA_LARP4 expression was associated with poor prognosis of PCa patients. The circular RNA_LARP4 was lowly expressed in PCa tissues compared with adjacent samples. The expression of circular RNA_LARP4 was downregulated in PCa cell lines. The cell migrated and invaded ability of PCa cells was inhibited after circular RNA_LARP4 was overexpressed. Furthermore, FOXO3A expression was increased via the overexpression of circular RNA_LARP4. Circular RNA_LARP4 could suppress cell migration and invasion of PCa by upregulating FOXO3A.