ABSTRACT
Objective:To explore the expression of signal sequence receptor subunit 1 (SSR1) and its prognostic value in hepatocellular carcinoma.Methods:Search the expression data and relevant clinical data of SSR1 in hepatocellular carcinoma patients from the Cancer Genome Atlas (TCGA) database to June 20, 2021, and download relevant public data. The expression levels of SSR1 in 334 cases of hepatocellular carcinoma with complete information and data were analyzed retrospectively. The expression difference of SSR1 gene between hepatocellular carcinoma and adjacent tissues was analyzed by Wilcoxon signed rank test. Patients with hepatocellular carcinoma were divided into high expression group and low expression group based on the median value of SSR1 expression level (14.660). χ 2 test was conducted to analyze the relationship between SSR1 expression and clinicopathological features. Cox regression and Log-rank survival test were used to analyze the relationship between SSR1 gene expression, clinicopathological features and overall survival rate in patients with hepatocellular carcinoma. Univariate and multivariate Cox regression analysis were used to determine the factors affecting prognosis. Gene set enrichment analysis (GSEA) was used to predict the possible regulatory pathways. Result:Bioinformatics analysis based on TCGA database showed that the expression level of SSR1 in hepatocellular carcinoma (16.320±7.231) was significantly higher than that in normal liver tissue (7.473±1.410). The difference between groups was statistically significant ( t=8.621, P<0.001).The overall survival rate of patients with high SSR1 gene expression group was lower than that of patients with high SSR1 gene expression group (χ 2=10.1, P<0.001). The high expression of SSR1 gene was related to sex (χ 2=4.392, P=0.036), Stage (χ 2=6.264, P=0.012), T stage (χ 2=4.561, P=0.033) and Grade classification (χ 2=14.015, P<0.001). Multivariate Cox regression analysis showed that patients with high expression of SSR1 gene got worse risk of death ( HR=1.030, 95% CI:1.002-1.060, P=0.036), and SSR1 gene expression was an independent predictor of hepatocellular carcinoma. Gene set enrichment analysis showed that the high expression of SSR1 was related to ubiquitination, cell cycle, RNA degradation, mTOR signal pathway, Wnt signal pathway and MAPK signal pathway. Conclusion:SSR1 gene is significantly up-regulated in hepatocellular carcinoma, which is related to gender, Stage, T stage and Grade classification. Ubiquitination, cell cycle, RNA degradation, mTOR signal pathway, Wnt signal pathway and MAPK signal pathway may be the key pathways for SSR1 to promote the occurrence and development of hepatocellular carcinoma.
ABSTRACT
Emerging studies have demonstrated that long noncoding RNAs (lncRNAs) play essential roles in tumorigenesis. However, the role and function of lncRNAs in hypopharyngeal squamous cell carcinoma (HSCC) have not been completely elucidated. The present study explored the function of a novel lncRNA, RP11156L14.1, in HSCC. RP11156L14.1 was revealed to be highly expressed in HSCC tissues and cell lines. Knockdown of RP11156L14.1 inhibited proliferation, migration, and invasion in HSCC cells. Furthermore, RP11156L14.1 regulated epithelialmesenchymal transition (EMT) by controlling EMTrelated protein expression. Mechanistically, RP11156L14.1 exerted its function as a competing endogenous RNA (ceRNA) and directly interacted with miR548ao3p. The present study also demonstrated that miR548ao3p regulated signal sequence receptor subunit 1 (SSR1) expression by targeting SSR1 3'UTR. Moreover, the xenograft HSCC tumor model revealed that knockdown of RP11156L14.1 markedly suppressed HSCC tumor growth in vivo. In summary, these findings indicated that the lncRNA RP11156L14.1 functions as an oncogene in HSCC by competing with miR548ao3p in regulating SSR1 expression. The RP11156L14.1/miR548ao3p/SSR1 axis could be utilized as a potential novel biomarker and therapeutic target for HSCC.
