Comprehensive analysis of N 6 ‐methyladenosine‐related long non‐coding RNAs for prognosis prediction in liver hepatocellular carcinoma

Aims: We aimed to find common and distinct molecular characteristics between LIHC and CHOL based on miRNA-TF-gene FFL. Background: Liver hepatocellular carcinoma (LIHC) and cholangiocarcinoma (CHOL) are two main histological subtypes of primary liver cancer with a unified molecular landscape, and feed-forward loops (FFLs) have been shown to be relevant in these complex diseases. Objective: To date, there has been no comparative analysis of the pathogenesis of LIHC and CHOL based on regulatory relationships. Therefore, we investigated the common and distinct regulatory properties of LIHC and CHOL in terms of gene regulatory networks. Method: Based on identified FFLs and an analysis of pathway enrichment, we constructed pathway-specific co-expression networks and further predicted biomarkers for these cancers by network clustering. Resul: We identified 20 and 36 candidate genes for LIHC and CHOL, respectively. The literature from PubMed supports the reliability of our results. Conclusion: Our results indicated that the hsa01522-Endocrine resistance pathway was associated with both LIHC and CHOL. Additionally, six genes (SPARC, CTHRC1, COL4A1, EDIL3, LAMA4 and OLFML2B) were predicted to be highly associated with both cancers, of which SPARC was significantly highly ranked. Other: In addition, we inferred that the Collagen gene family, which appeared more frequently in our overall prediction results, might be closely related to cancer development.

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Identification of glycolysis related pathways in pancreatic adenocarcinoma and liver hepatocellular carcinoma based on TCGA and GEO datasets

Cancer Cell International ◽

10.1186/s12935-021-01809-y ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Ji Li ◽

Chen Zhu ◽

Peipei Yue ◽

Tianyu Zheng ◽

Yan Li ◽

...

Keyword(s):

Gene Expression ◽

Hepatocellular Carcinoma ◽

Energy Metabolism ◽

Pancreatic Adenocarcinoma ◽

Digestive System ◽

Prognostic Significance ◽

R Package ◽

The Cancer Genome Atlas ◽

System Structure ◽

Liver Hepatocellular Carcinoma

Abstract Background Abnormal energy metabolism is one of the characteristics of tumor cells, and it is also a research hotspot in recent years. Due to the complexity of digestive system structure, the frequency of tumor is relatively high. We aim to clarify the prognostic significance of energy metabolism in digestive system tumors and the underlying mechanisms. Methods Gene set variance analysis (GSVA) R package was used to establish the metabolic score, and the score was used to represent the metabolic level. The relationship between the metabolism and prognosis of digestive system tumors was explored using the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Volcano plots and gene ontology (GO) analyze were used to show different genes and different functions enriched between different glycolysis levels, and GSEA was used to analyze the pathway enrichment. Nomogram was constructed by R package based on gene characteristics and clinical parameters. qPCR and Western Blot were applied to analyze gene expression. All statistical analyses were conducted using SPSS, GraphPad Prism 7, and R software. All validated experiments were performed three times independently. Results High glycolysis metabolism score was significantly associated with poor prognosis in pancreatic adenocarcinoma (PAAD) and liver hepatocellular carcinoma (LIHC). The STAT3 (signal transducer and activator of transcription 3) and YAP1 (Yes1-associated transcriptional regulator) pathways were the most critical signaling pathways in glycolysis modulation in PAAD and LIHC, respectively. Interestingly, elevated glycolysis levels could also enhance STAT3 and YAP1 activity in PAAD and LIHC cells, respectively, forming a positive feedback loop. Conclusions Our results may provide new insights into the indispensable role of glycolysis metabolism in digestive system tumors and guide the direction of future metabolism–signaling target combined therapy.

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