ArticleDigestive diseases and sciences2024
E2F5 Targeted by Let-7d-5p Facilitates Cell Proliferation, Metastasis and Immune Escape in Gallbladder Cancer.
Article in Digestive diseases and sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Proteomic Analysis Identifies Potential Biomarkers of ELOC -Mutated Renal Cell Carcinoma.The American journal of surgical pathology · 2026Article
- Fu Zheng Xiao Yu San Jie Decoction affects the proliferation of renal cell carcinoma via regulatingTranslational andrology and urology · 2025Article
- Tumor immune evasion and the Let-7 family: insights into mechanisms and therapies.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
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5 authors at 2 institutions in 1 country.
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Abstract
backgroundGallbladder 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.
aimsTo explore the regulatory functions of E2F5 and its related molecular regulatory mechanism in GBC progression.
methodsThe 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
resultsIn 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.
conclusionE2F5 targeted by let-7d-5p facilitated cell proliferation, metastasis and immune escape in GBC through the JAK2/STAT3 pathway.
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