RESUMEN
OBJECTIVE: Citron Rho-interacting serine/threonine kinase (CIT) was identified recently as an oncogene involved in the progression of various malignant tumors, but its role in prostate cancer (PCa) remains unclear. In this study, we aimed to investigate the biological functions of CIT in PCa. METHODS: We analyzed the expression of CIT in PCa tissues and its clinical correlations based on the Cancer Genome Atlas (TCGA) and Memorial Sloan-Kettering Cancer Center (MSKCC) dataset. We then examined the effects of RNA interference-mediated CIT silencing on the proliferation, migration and invasion of PC-3 cells using cell counting kit-8, wound healing assay and Transwell assay. We also investigated the effect of CIT silencing on epithelial-mesenchymal transition (EMT) and Hippo-Yap signaling pathway in the cells using Western blotting. RESULTS: CIT expression was significantly elevated in PCa tissues from TCGA cohort (P < 0.05). MSKCC dataset analysis showed that an elevated expression of CIT was significantly correlated with N stage (P=0.001), distant metastasis (P < 0.001), Gleason score (P=0.010) and PSA (P=0.004). In cultured PC-3 cells, knockdown of CIT significantly inhibited cell proliferation, migration and invasion, reversed the EMT phenotype and decreased the expression and activity of YAP. CONCLUSIONS: CIT might function as an oncogene in PCa by modulating the Hippo-YAP signaling pathway and serve as a candidate therapeutic target for PCa.
Asunto(s)
Neoplasias de la Próstata , Proteínas Adaptadoras Transductoras de Señales , Línea Celular Tumoral , Movimiento Celular , Proliferación Celular , Vía de Señalización Hippo , Humanos , Masculino , Metástasis de la Neoplasia , Fosfoproteínas , Proteínas Serina-Treonina Quinasas , Serina , Transducción de Señal , Factores de Transcripción , Proteínas Señalizadoras YAPRESUMEN
OBJECTIVE@#Citron Rho-interacting serine/threonine kinase (CIT) was identified recently as an oncogene involved in the progression of various malignant tumors, but its role in prostate cancer (PCa) remains unclear. In this study, we aimed to investigate the biological functions of CIT in PCa.@*METHODS@#We analyzed the expression of CIT in PCa tissues and its clinical correlations based on the Cancer Genome Atlas (TCGA) and Memorial Sloan-Kettering Cancer Center (MSKCC) dataset. We then examined the effects of RNA interference-mediated CIT silencing on the proliferation, migration and invasion of PC-3 cells using cell counting kit-8, wound healing assay and Transwell assay. We also investigated the effect of CIT silencing on epithelial-mesenchymal transition (EMT) and Hippo-Yap signaling pathway in the cells using Western blotting.@*RESULTS@#CIT expression was significantly elevated in PCa tissues from TCGA cohort ( < 0.05). MSKCC dataset analysis showed that an elevated expression of CIT was significantly correlated with N stage (=0.001), distant metastasis ( < 0.001), Gleason score (=0.010) and PSA (=0.004). In cultured PC-3 cells, knockdown of CIT significantly inhibited cell proliferation, migration and invasion, reversed the EMT phenotype and decreased the expression and activity of YAP.@*CONCLUSIONS@#CIT might function as an oncogene in PCa by modulating the Hippo-YAP signaling pathway and serve as a candidate therapeutic target for PCa.