Digestive diseases and sciences · 2023
E2F5 Targeted by Let-7d-5p Facilitates Cell Proliferation, Metastasis and Immune Escape in Gallbladder Cancer.
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Chen Lei, Guo Songyi, Zhang Dafang, Li Xinyu, Chen Jianfei
Аннотация
BACKGROUND: Gallbladder cancer (GBC) remains a serious cause of cancer-related mortality across the globe. E2F5 has been identified to as a known oncogene in various cancers. However, the special functions of E2F5 have not been investigated in GBC.
AIMS: To explore the regulatory functions of E2F5 and its related molecular regulatory mechanism in GBC progression.
METHODS: The expression of genes were examined through qRT-PCR, western blot and IHC assay. The cell proliferation was assessed through CCK-8 and EDU assays. The cytotoxicity was tested through LDH assay. The percentage of CD8+ T cells and cell apoptosis were evaluated through flow cytometry. The binding ability was detected through luciferase reporter assay. The tumor growth was assessed through in vivo assays.
RESULTS: In this study, it was demonstrated that E2F5 expression was evaluated in GBC, and resulted into poor prognosis. Bioinformatics analysis revealed E2F5 as a target for let-7d-5p, which when overexpressed, suppressed the metastasis and proliferation of GBC through the downregulation of E2F5. It was discovered that E2F5 activates JAK2/STAT3 signaling which is suppressed by let-7d-5p, implicating this pathway as one of the effectors of the oncogenic effects of ESF5 in GBC. E2F5 had been confirmed to aggravate tumor growth in vivo.
CONCLUSION: E2F5 targeted by let-7d-5p facilitated cell proliferation, metastasis and immune escape in GBC through the JAK2/STAT3 pathway.
AIMS: To explore the regulatory functions of E2F5 and its related molecular regulatory mechanism in GBC progression.
METHODS: The expression of genes were examined through qRT-PCR, western blot and IHC assay. The cell proliferation was assessed through CCK-8 and EDU assays. The cytotoxicity was tested through LDH assay. The percentage of CD8+ T cells and cell apoptosis were evaluated through flow cytometry. The binding ability was detected through luciferase reporter assay. The tumor growth was assessed through in vivo assays.
RESULTS: In this study, it was demonstrated that E2F5 expression was evaluated in GBC, and resulted into poor prognosis. Bioinformatics analysis revealed E2F5 as a target for let-7d-5p, which when overexpressed, suppressed the metastasis and proliferation of GBC through the downregulation of E2F5. It was discovered that E2F5 activates JAK2/STAT3 signaling which is suppressed by let-7d-5p, implicating this pathway as one of the effectors of the oncogenic effects of ESF5 in GBC. E2F5 had been confirmed to aggravate tumor growth in vivo.
CONCLUSION: E2F5 targeted by let-7d-5p facilitated cell proliferation, metastasis and immune escape in GBC through the JAK2/STAT3 pathway.