Prognostic value and mechanism of EPHB2 overexpression in cervical cancer

Abstract

Background Cervical cancer (CC) still represents an important challenge for female malignant tumors. In recent years, increasing evidence has indicated that EPHB2 plays a significant part in the origin and progression of many types of cancer in humans. Nevertheless, the mechanism of EPHB2 in CC remains inexplicable. The purpose of this study is to determine the prognostic value and related regulatory mechanism of EPHB2 in CC. Methods The basic clinical information and transcriptome data related to CC patients were downloaded from TCGA database and conducted standardization processing. TIMER2.0 was used for analyzing the EPHB2 expression differences of between 38 cancer types and corresponding normal tissues. The expression and prognostic value (including OS and RFS) of EPHB2 in different cancer types were determined by GEPIA2. And the starbase database was used for exploring the upstream miRNAs and lncRNAs of EPHB2. Then, The correlation analysis of EPHB2, miRNA and lncRNA and the exploration of prognostic value and expression of miRNAs in CESC was conducted using the R language packages. We also analyzed the prognostic value and expression difference of 187 lncRNAs based on the UALCAN database. Finally, we performed the correlation analysis between EPHB2 and multiple immune cells using the R language package. Results In our study, the AC073957.3/hsa-miR-150-5p axis was found to be the most potential upstream ncRNA-related regulator of EPHB2 in CC. And the results of immune correlation infiltration analysis suggest that as EPHB2 copy numbers fluctuate in CESC there is an obvious difference in immune cell infiltration levels, and EPHB2 was markedly positively correlated with Th2 cell, NK cell, Eosinophils, Tgd, Mast cell, NK CD56bright cells and Tem while negatively correlated with Tcm and B cell in CC. Conclusion Our study shows that EPHB2 is a potential prognostic marker, and its overexpression is related to poor prognosis of CC, which is expected to be a new therapeutic target for CC.