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Identification of CT-Detected extramural vessel invasion related gene regulatory network

ABSTRACT: Gastric cancer (GC) was a worldwide cancer with high heterogeneity. More than 90% of GC patients in clinical practice were advanced GC, and the radical resection rate was only about 50%. For advanced gastric cancer, there is no specific targeted therapeutic regimen and the prognosis is poor. Extramural vessel invasion(EMVI) was identified as the tumor cells infiltrating through the gastric wall and into the lumen of extramural vessel. CT detected EMVI has been tested as the independent risk factor of the synchronous metastasis and long-term survival. The development of EMVI was believed as a defining characteristic of gastrointestinal cancer in advanced stage. In recent years, approaches and promising results arising from correlation of cancer imaging features with high-throughput data lead to the new research area known as radiogenomics. A significant amount of literatures in radiogenomics are promising to increase precision in diagnosis, assessment of prognosis and prediction of oncologic treatment . In the present study, we performed a CT detected EMVI related gene regulatory network analysis of differentially expressed coding genes in locally advanced GC. We screened the mRNA and their respective gene networks that were involved in the progression of CT detected EMVI.

ORGANISM(S): Homo sapiens

PROVIDER: GSE182831 | GEO | 2023/01/11

REPOSITORIES: GEO

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Project description:Background: Helicobacter pylori (HP) infection may initiate and promote progression of gastric carcinogenesis. ONECUT2 shows promise for tumor diagnosis, prognosis, and treatment. This study explored ONECUT2's role and specific mechanism underlying HP infection-associated gastric carcinogenesis to suggest a basis for targeting ONECUT2 as a therapeutic strategy for gastric cancer (GC). Methods: Public data, single-cell RNA sequencing, spatial transcriptome analysis, RNA sequencing, GC tissue specimens, and clinical survival data were analyzed. Human GC organoids, HP infection, 3D sphere-forming, and extreme-dilution nude mouse models were constructed. Western blotting, qPCR, immunohistochemical staining, dual-luciferase reporter assays, phosphokinase microarray, and immunofluorescence were used. Results: Multidimensional data supported an association between ONECUT2, HP infection, and GC pathogenesis. HP infection upregulated ONECUT2 transcriptional activity via NFκB. In vitro and in vivo experiments demonstrated that ONECUT2 increases stemness in GC cells. ONECUT2 was also shown to inhibit PPP2R4 transcription, resulting in reduced PP2A activity, which in turn increased AKT/β-catenin phosphorylation. AKT/β-catenin phosphorylation facilitates β-catenin translocation to the nucleus, initiating transcription of downstream stemness-associated genes in GC cell. HP infection could upregulate the phosphorylation of AKT and β-catenin triggered by ONECUT2 downregulation via induction of ONECUT2. Clinical survival analysis indicated that high ONECUT2 expression might be an indicator of poor prognosis in GC. Conclusion: This study highlights a critical role played by ONECUT2 in promoting HP infection-associated GC by enhancing cell stemness through the PPP2R4/AKT/β-catenin signaling pathway. These findings suggest promising therapeutic strategies and potential therapeutic targets for GC treatment. Keywords: Helicobacter pylori; gastric cancer; prognosis; tumor stemness; ONECUT2

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Identification of CT-Detected extramural vessel invasion related gene regulatory network

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