Journal
DIGESTIVE AND LIVER DISEASE
Volume 54, Issue 7, Pages 937-945Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.dld.2021.09.003
Keywords
E2F5; Gastric cancer; Proliferation and invasion; Transcriptional regulation; UBE2T
Categories
Funding
- Science and Technology Innovation Project of Higher Education of Shanxi Province [2019L0679]
- Research Youth Startup Fund Project of Heping Hospital [HPYJ201929]
- Changsha Municipal Natural Science Foundation [kq2014024]
- Scientific research project of Hunan Provincial Health Commission [202102060121]
- Science and Technology Plan Project of Hunan Province [2020ZK4013]
- Educational Commission of Hunan Province of China [19K101]
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This study confirmed for the first time the upregulation of E2F5 in gastric cancer and discovered that E2F5 can directly upregulate UBE2T transcription, thereby promoting malignant progression.
The underlying mechanisms of E2F5 upregulation and its pro-tumor functions have not been elucidated in gastric cancer (GC). Here, the expression, prognostic value, mutation status, and promoter methylation of E2F5 were evaluated. The effects of E2F5 depletion on cell proliferation and invasion in GC, were also assessed through in vitro experiments. Additionally, gene set enrichment analysis (GSEA) was applied to analyze the potential downstream regulator of E2F5. The study also assessed the correlation and transcription regulation between E2F5 and UBE2T. Finally, the roles of UBE2T in E2F5-related pro-tumor functions were examined. The findings revealed that E2F5 was upregulated and showed remarkable association with pathological variables and prognosis. Hypomethylation of the E2F5 promoter predicted poor prognosis and partially caused E2F5 upregulation in GC. E2F5 knockdown significantly inhibited the proliferation and invasion of GC cells. E2F5 had a significant positive correlation with UBE2T in GC. Mechanistically, E2F5 promoted UBE2T transcription and UBE2T overexpression reversed the effects of E2F5 depletion on the proliferation and invasion of cells in GC. Taken together, this study originally confirmed the upregulation of E2F5 in GC, revealed that E2F5 can directly upregulate UBE2T transcription, and subsequently promote the malignant progression, which highlights that the E2F5/UBE2T axis can potentially be used in the diagnosis and treatment of GC. (C) 2021 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
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