Abstract

Reptin/RUVBL2 is involved in the remodeling of chromatin, DNA damage repair, and regulation of the cell cycle, all of which help to play essential roles in cancer. However, relevant pan-cancer analysis of Reptin is lacking. This study first investigated the potential oncogenic roles of Reptin and revealed a relationship between Reptin with clinicopathological characteristics and immune infiltration based on big data. Here, we showed that Reptin is overexpressed in many cancers. A significant association exists between the expression of Reptin and the prognosis of cancer cases. Reptin had a meaningful interaction with the immune infiltration of CD4+ Th1 cells and immune modulator genes in multiple cancer types. And negative correlation exists between Reptin and cancer-associated fibroblasts in BRCA, PRAD, TGCT, and THYM. A significant negative association exists between Reptin and regulatory T cells in TGCT and THCA. Moreover, Reptin is significantly associated with genomic heterogeneity, DNA mismatch repair genes, methyltransferase, and RNA modification genes in specific cancer types. Spliceosome, Hippo signaling pathway, DNA replication pathway, and acetyltransferase activity-associated functions were observed in the effect of Reptin on the tumor. This systematic analysis highlights Reptin as a vital cancer regulator among numerous genes and proved its potential prognosticator value and therapeutic target role for specific tumor types.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.