Cell division cycle associated 7 like predicts unfavorable prognosis and promotes invasion in glioma

Abstract

BackgroundCell division cycle associated 7 like (CDCA7L) belongs to the JPO protein family, which is recently identified as a target gene of c-Myc and is frequently dysregulated in multiple cancers. This study aimed to explore the clinicpathological value and biological role of CDCA7L in glioma. MethodsCDCA7L expression in glioma patients was determined using the Oncomine database, and the prognostic role of CDCA7L expression was assessed in a retrospective cohort study. Moreover, the relationship of CDCA7L expression with the clinicopathological characteristics in glioma patients, including age, gender, tumor size, cystic change, Karnofsky performance scale (KPS) score, tumor location, extent of resection, WHO grade, adjuvant therapy and tumor recurrence, was analyzed in this study. In addition, the CDCA7L small interfering (si) RNA was constructed and transfected into the glioma U251 cells, so as to examine the role of CDCA7L in glioma patients. Besides, the changes in U251 cell invasion after transfection with CDCA7L siRNA were also monitored through Transwell assay. ResultsOur results suggested that CDCA7L expression was up-regulated in different glioma types, including glioblastoma, oligodendroglioma, diffuse astrocytoma and anaplastic astrocytoma. Moreover, the current retrospective cohort study indicated that high CDCA7L expression was associated with tumor size, WHO grade, adjuvant therapy and recurrence, as well as the poor overall survival (OS) and recurrence-free survival (RFS) in glioma patients. Lastly, CDCA7L expression was knocked down using CDCA7L siRNA, which could block the invasion abilities of glioma U251 cells. ConclusionsCDCA7L is highly expressed in human glioma tissues and a high CDCA7L expression level predicts the dismal prognosis for glioma patients. Moreover, CDCA7L can promote glioma invasion, which can serve as an independent potential prognostic biomarker for glioma patients.