Small Nucleolar RNA, C/D Box 15B Regulates The TRIM25/P53 Complex To Promote The Development Of Endometrial Cancer

Background: Endometrial cancer is associated with a high mortality rate,which warrants the identification of novel diagnostic markers and therapeutic targets.The aim of this study is to evaluate the role of SNORD15 B in the development of endometrial cancer and explore the potential underlying mechanisms.Methods: Bioinformatics was used to analyze the expression level and prognostic relevance of SNORD15 B in endometrial cancer.The Ishikawa and HEC-1B cells were respectively transfected with SNORD15 B expression plasmid and anti-sense oligonucleotide,or the corresponding empty vector and non-specific sequence.The malignant phenotype of the suitably transfected cells was assessed by the standard in vitro functional assays and the establishment of in vivo xenografts.The expression levels of specific markers were analyzed with RT-q PCR and Western blotting.The sub-cellular localization of P53 was determined by analyzing the nuclear and cytoplasmic fractions.RIP,Co-IP and immunohistochemistry were performed as per standard protocols.Results: SNORD15 B was overexpressed in the endometrial cancer tissues and correlated to a poor prognosis.Ectopic expression of SNORD15 B in Ishikawa cells inhibited apoptosis,increased the proliferation,invasion and migration in vitro,and enhanced their tumorigenicity in vivo.SNORD15 B overexpression also upregulated TRIM25 and accelerated P53 accumulation in the cytoplasm of the endometrial cancer cells.Conclusion: SNORD15 B functions as an oncogene in endometrial cancer by targeting the TRIM25/P53 complex and blocking the nuclear translocation of P53.