Background Several studies have demonstrated autophagy was involved in the process of esophageal adenocarcinoma (EAC). The aim of this study was to explore autophagy-related genes (ARGs) correlated with overall survival (OS) in EAC patients. Methods Expressions of ARGs in EAC and normal samples were downloaded from TCGA database. GO and KEGG enrichment analyses were used to investigate the ARGs bioinformatics functions. Univariate and multivariate cox regressions were performed to identify prognostic ARGs and the independent risk factors. ROC curve was established to evaluate the feasibility to predict the prognosis. Finally, the correlations between ARGs and clinical features were further explored. In addition, significantly different ARGs were verified in EAC specimens and normal esophageal mucosal tissues. Results Thirty significantly different ARGs were selected from EAC and normal tissues. Functional enrichments showed these ARGs were mainly related apoptosis. Multivariate cox regression analyses demonstrated eight ARGs were significantly associated with OS. Among these eight genes, BECN1 (HR = 0.321, P = 0.046), DAPK1 (HR = 0.636, P = 0.025) and CAPN1 (HR = 0.395, P = 0.004) played protective roles in survival. Gender (HR = 0.225, P = 0.032), stage (HR = 5.841, P = 0.008) and risk score (HR = 1.131, P < 0.001) were independent prognostic risk factors. ROC curves showed better efficacy to predict survival using the risk score. Additionally, we found BECN1, DAPK1, VAMP7 and SIRT1 genes were correlated significantly with survival status, gender, primary tumor and tumor stage (all P < 0.05). The experimental results confirmed the BIRC5 was overexpressed and the ITPR1, PRKN were downregulated in the EAC tissues compared with the normal esophageal mucosal tissues (all P < 0.05). Conclusion Our findings suggested that autophagy was involved in the process of EAC. Several ARGs probably could serve as diagnostic and prognostic biomarkers and may help facilitate therapeutic targets in EAC patients.

Eukaryotic translation initiation factor 4 gamma 1 (EIF4G1) is highly expressed in many cancers and affects their occurrence and development. However, the effect of EIF4G1 on the prognosis, biological function and the relevant mechanism in lung squamous cell carcinoma (LSCC) is unclear. Through clinical cases, Cox’s proportional hazard model and Kaplan–Meier plotter survival analysis, we find the expression levels of EIF4G1 are dependent on age and clinical stage, high expression of EIF4G1 could be used to predict the overall survival of LSCC patients. LSCC cell line NCI-H1703, NCI-H226 and SK-MES-1infected with EIF4G1 siRNA are used to detect the function of EIF4G1 with cell proliferation and tumorigenesis in vivo and vitro. The data show that EIF4G1 promotes tumor cell proliferation and the G1/S transition of cell cycle in LSCC, then the biological function of LSCC is effected by the AKT/mTOR pathway. Above all, these results have demonstrated that EIF4G1 promotes LSCC cell proliferation and may represent an indicator of prognosis in LSCC.

Background Lung adenocarcinoma is one of the common causes of cancer‐related deaths worldwide. Histone cluster 1 H2A family member b (HIST1H2AB) is a member of the histone H2A family. Bioinformatic analyses have revealed that HIST1H2AB is highly expressed in some cancers and might be an oncogene. However, information on the function of HIST1H2AB in lung adenocarcinoma is limited. Methods The expression of HIST1H2AB was analyzed in normal lung, lung adenocarcinoma and paracancerous tissues from The Cancer Genome Atlas (TCGA) database and immunohistochemistry staining. It was further verified in the relative cell lines using real‐time quantitative polymerase chain reaction (RT‐qPCR). When the adenocarcinoma cells lines (A549 and H1299) were successfully transfected with shHIST1H2AB or an empty plasmid packaged into a lentivirus, cell proliferation was detected using Celigo fluorescence cell‐counting, colony formation and annexin V‐allophycocyanin assays. Twenty nude mice were subcutaneously injected with A549 cells transfected with shHIST1H2AB or empty plasmid; the tumor size was recorded on day 25 and then measured every 3 days thereafter. The final tumor weight was measured on day 37. Significantly differentially expressed genes were analyzed using a human gene expression array. Furthermore, the potentially relevant genes were verified using RT‐qPCR and western blotting. Results HIST1H2AB was highly expressed in lung adenocarcinoma tissues from TCGA database and immunohistochemistry staining. Similar results were seen in the lung adenocarcinoma cells. When the cells were successfully transfected with shHIST1H2AB or an empty plasmid, downregulation of HIST1H2AB inhibited the growth and promoted the apoptosis of lung adenocarcinoma cells. The xenograft results suggested that HIST1H2AB downregulation delayed tumor growth and reduced tumor weight. Moreover, interferon signaling pathway and four genes (HMGB1, FOXM1, F2RL1 and SLC4A7) might be regulated by HIST1H2AB in the development of lung adenocarcinoma as indicated through gene expression array, RT‐qPCR and western blotting analyses. Conclusions HIST1H2AB acts as an oncogenic protein and HIST1H2AB inhibition suppresses the proliferation of lung adenocarcinoma cells. It may be a novel target for lung adenocarcinoma therapy.

Background: Autophagy plays a vital role in cancer development. However, the prognostic value of autophagy-related genes (ARGs) in low-grade gliomas (LGG) is unclear. This research aimed to investigate whether ARGs correlated with overall survival (OS) in LGG patients.Methods: RNA-sequencing data were obtained from The Cancer Genome Atlas (TCGA) TARGET GTEx database. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis of ARGs were performed by the “clusterprofile” R package. Cox regression with the wald χ2 test was employed to identify prognostic significant ARGs. Next, the receiver operator characteristic curves were established to evaluate the feasibility of risk score (riskscore=h0(t)exp(∑j=1nCoefj×Xj)) and other clinical risk factors to predict prognosis. A nomogram was constructed. Correlations between clinical features and ARGs were further verified by a t-test or Kruskal–Wallis test. In addition, the correlations between autophagy and immune cells were assessed through the single-sample gene set enrichment analysis (ssGSEA) and tumor immune estimation resource database. Last, the prediction model was verified by LGG data downloaded from the Chinese Glioma Genome Atlas (CGGA) database.Results: Overall, 35 DE-ARGs were identified. Functional enrichment analysis showed that these genes were mainly related to oxidative stress and regulation of autophagy. Nine ARGs (BAX, BIRC5, CFLAR, DIRAS3, GRID2, MAPK9, MYC, PTK6, and TP53) were significantly associated with OS. Age (Hazard ratio (HR) = 1.063, 95% CI: 1.046–1.080), grade (HR = 3.412, 95% CI: 2.164–5.379), histological type (HR = 0.556, 95% CI: 0.346–0.893), and risk score (HR = 1.135, 95% CI: 1.104–1.167) were independent prognostic risk factors (all p &lt; 0.05). In addition, BIRC5, CFLAR, DIRAS3, TP53, and risk scores were found to correlate significantly with age and tumor grade (all p &lt; 0.05). Immune cell enrichment analysis demonstrated that the types of immune cells and their expression levels in the high-risk group were significantly different from those in the low-risk group (all p &lt; 0.05). A prognostic nomogram was constructed to predict 1-, 3-, and 5-year survival, and the prognostic value of sorted ARGs were verified in the CGGA database and clinical samples.Conclusion: Our findings suggest that the 9 DE-ARGs’ risk score model could serve as diagnostic and prognostic biomarkers. The prognostic nomograms could be useful for individualized survival prediction and improved treatment strategies.