Purpose: Liver cancer is a high mortality disease with no curable treatments. Posttranscriptional modifications play essential roles in the occurrence and the progression of liver cancer. EIF2B5 is a subunit of EIF2B that regulates the initiation and the rate of translation and participates in several diseases including tumors. This study aims to elucidate the prognostic significance of EIF2B5 in liver cancer.
Materials and methods: We used The Cancer Genome Atlas database to analyze the expression of EIF2B5 in liver cancer. Then we used chi-squared and Fisher exact tests to test the correlation between clinical characteristics and EIF2B5 expression. Finally, we assessed the role of EIF2B5 in prognosis by Kaplan–Meier curves and Cox analysis. Gene set enrichment analysis was performed by using The Cancer Genome Atlas data set. Results: The results showed that EIF2B5 was upregulated in liver cancer, and the expression was related to histologic grade, clinical stage, and vital status. Moreover, Kaplan–Meier curves and Cox analysis implicated that highly expressed EIF2B5 correlated with poor prognosis, and EIF2B5 was an independent risk factor for liver cancer. Gene set enrichment analysis showed that ATR and BRCA pathway, cell cycle pathway, DNA repair, myc signaling pathway, and E2F targets are differentially enriched in EIF2B5 high-expression phenotype. Conclusion: Our results suggest that EIF2B5 participated in cancer progression and could become a biomarker for the prognosis of patients with liver cancer.

FAM64A, a marker of cell proliferation, has been investigated as a potential biomarker in several cancers. In the present study, we examined the value of FAM64A expression in the diagnosis and prognosis of pancreatic cancer through bioinformatics analysis of data obtained from The Cancer Genome Atlas (TCGA) database. The diagnostic value of FAM64A expression in pancreatic cancer tissue was deteremined through receiver operating characteristic (ROC) curve analysis, and based on the obtained cut-off value, patients were divided into two groups (high FAM64A expression and low FAM64A expression). Chi-square and Fisher exact tests were applied to identify associations between FAM64A expression and clinical features. Moreover, the effect of FAM64A expression in the survival of pancreatic cancer patients was observed by Kaplan-Meier and Cox analyses. Gene set enrichment analysis (GSEA) was performed using the TCGA dataset. Our results showed that high FAM64A expression in pancreatic cancer was associated with survival status, overall survival (OS), and recurrence. The area under the ROC curve was 0.736, which indicated modest diagnostic value. Patients with higher FAM64A expression had significantly shorter OS and recurrence-free survival (RFS) times. Multivariate survival analysis demonstrated that high FAM64A expression was an independent risk factor for OS and RFS. GSEA identified mitotic spindles, myc targets, MTORC1 signaling, G2M checkpoint, E2F targets, DNA repair, glycolysis and unfolded protein response as differentially enriched with the high FAM64A expression phenotype. In conclusion, high FAM64A mRNA expression is an independent risk factor for poor prognosis in pancreatic cancer.

Pancreatic cancer is one of the most malignant tumors worldwide. DNA replication plays a critical role in the occurrence and development of pancreatic cancer. TYMS encodes thymidylate synthase, which is important for DNA synthesis. The TYMS gene has been assessed in some tumors. However, the specific role of TYMS in pancreatic cancer has not been identified. This study was designed to clarify the diagnostic and prognostic significance of TYMS in pancreatic cancer. The Cancer Genome Atlas (TCGA) database was used to compare TYMS expression in pancreatic cancer, and ROC curve analysis was used to investigate its diagnostic value. The correlation between clinical characteristics and TYMS expression was analyzed, and the prognostic value of TYMS expression in the patients with pancreatic cancer was assessed by Kaplan–Meier curves and Cox analysis. TYMS was upregulated in pancreatic cancer and associated with poor overall survival (OS) and recurrence-free survival (RFS). Univariate and multivariate survival analysis demonstrated that TYMS is an independent risk factor for OS and RFS in patients with pancreatic cancer. The upregulation of TYMS in pancreatic cancer leads to unfavorable OS and RFS in patients, and represents a diagnostic and prognostic biomarker for patients with pancreatic cancer.

Purpose: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in the clinic all over the world, which has become a public health challenge. The T/N/M staging system plays a core role in HCC prognosis. However, it cannot precisely stratify the risk of HCC prognosis. MiR-454-3p plays an important role in the progression of tumors. Therefore, we need to develop more reliable prognostic markers for HCC patients which can focus on miR-454-3p. Methods: We used Chi-square and Fisher exact tests to assess correlations between miR-454-3p expression and clinical parameters in liver cancer patients from The Cancer Genome Atlas database (TCGA). Then, Cox regression analysis, Kaplan-Meier curve, and log-rank test were used to compare the difference of survival between the high-expression group and low-expression group, and P value was included. Finally, we used TCGA data set to carry out gene enrichment analysis. Results: In this research, the expression of miR-454-3p increased in HCC and was associated with patient survival, G3/G4 staging, III/IV staging and T staging. Higher miR-454-3p expressed patients had shorter survival time. Besides, mitotic spindle, G2M checkpoint, and E2F targets were differentially enriched in miR-454-3p high-expression phenotype by Gene set enrichment analysis. Conclusion: Overexpression of miR-454-3p may be a significant and independent predictor of poor prognosis in HCC patients.

Background and Objective. Liver cancer is a highly malignant tumor, and patients typically have poor prognoses. Metabolic reprogramming is a hallmark of cancer, and downregulation of oxoglutarate dehydrogenase-like (OGDHL) contributes to the onset and progression of several cancers. We examined the role of altered OGDHL expression in liver cancer and determined its value as a diagnostic and prognostic indicator for patients. Material and Methods. R (version 3.5.1) and several R extensions were used for data mining of The Cancer Genome Atlas (TCGA) dataset (including RNAseq and clinical information) and statistical analysis. Receiver operating characteristic analysis was used to determine the diagnostic value of OGDHL. The chi-squared test was used to identify the clinical correlates of OGDHL downregulation. Survival analysis (with the log-rank test) and univariate and multivariate Cox analysis were used to evaluate the effect of OGDHL expression on overall survival (OS) and relapse-free survival. TCGA was used for analysis of gene set enrichment. Results. OGDHL had lower expression in cancerous liver tissues than noncancerous adjacent tissues, and low expression correlated with more advanced patient age, histologic grade, stage, T classification, and poor survival. Patients with lower OGDHL expression had shorter OS and relapse-free survival. Multivariate Cox regression indicated that low OGDHL expression was an independent risk factor for poor prognosis. Gene set enrichment analysis indicated enrichment of the mitotic spindle, G2M checkpoint, and E2F targets in the OGDHL low expression phenotype. Conclusion. OGDHL has potential as a diagnostic and prognostic biomarker for liver cancer.