Affiliation:
1. Department of Hepatobiliary surgery, Clinical Medical College, Yangzhou University
2. Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University
Abstract
Abstract
Background The regulator of ribosome synthesis 1 (RRS1) is a conserved nuclear protein in eukaryotes and is involved in the biological processes of a variety of tumors. However, its clinical significance in hepatocellular carcinoma (HCC) has not been completely elucidated. Methods To clarify the prognostic and diagnostic value of RRS1 in HCC patients by studying the relevant data of RRS1. TCGA data and GSE14520 database were used to clarify the expression and prognostic value of RRS1 in HCC. The common differentially expressed genes (DEGs) of RRS1 in HCC were screened, and further enrichment analysis of DEGs was performed. Next, we investigated the ceRNA regulatory mechanism of RRS1 and the correlation of RRS1 expression with cuproptosis related genes, immune microenvironment and cell cycle signaling pathway. Finally, immunohistochemical analysis of HCC tissue and normal liver tissue and cell proliferation assay of Hepatocellular carcinoma cells were performed. Results In our study, we found that the RRS1 high expression is closely related to poor prognosis. The enrichment analysis founded that many DEGs were enriched in cell cycle, response to copper ion, and regulation of adaptive immune response. Studies on the regulatory mechanism of ceRNA network make cleared that RRS1 expression was up-regulated in HCC by SNHG3/hsa-miR-216a-5p/RRS1 axis. Moreover, RRS1 may affect the progression of HCC patients through adjusting cuproptosis related genes, immune microenvironment and cell cycle signaling pathway. Finally, I demonstrated that RRS1 was highly expressed in HCC tissues by immunohistochemistry. Cell proliferation assay showed that RRS1 knockdown significantly inhibited the proliferation of HepG2 cells and HCC LM3. Conclusions Altogether, RRS1 can serve as a new prognostic and diagnosis biomarker for HCC patients, and RRS1 knockdown significantly inhibited the proliferation of HCC.
Publisher
Research Square Platform LLC