ArticleCancer management and research2020
Regulation of E2F Transcription Factor 3 by microRNA-152 Modulates Gastric Cancer Invasion and Metastasis.
Article in Cancer management and research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Regulation and function of microRNA-152 in various types of cancers: its upstream regulators and downstream targets.Clinical and experimental medicine · 2025Review
- Bioinformatics analysis of downstream circRNAs and miRNAs regulated by Runt-related transcription factor 1 in papillary thyroid carcinoma.Gland surgery · 2022Article
- miR-1297 inhibits osteosarcoma cell proliferation and growth by targeting CCND2.American journal of cancer research · 2022Article
- Circ_PGPEP1 Serves as a Sponge of miR-1297 to Promote Gastric Cancer Progression via Regulating E2F3.Digestive diseases and sciences · 2021Article
- MiR-573 suppresses cell proliferation, migration and invasion via regulation of E2F3 in pancreatic cancer.Journal of Cancer · 2021Article
- Comprehensive Analysis of E2F Family Members in Human Gastric Cancer.Frontiers in oncology · 2021Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe transcription factor, E2F transcription factor 3 (E2F3), has been proved to modulate metastasis in multiple human cancers. The present study was aimed to expound the function and specific mechanism of E2F3 in gastric cancer (GC) progression. MATERIALS AND
methodsThe expression of E2F3, microRNA-152 (miR-152) and PLK1 (polo-like kinase 1) in GC cell lines was detected by quantitative RT-PCR and Western blot. The roles of E2F3 and miR-152 in GC metastasis were classified using gain-of-function and loss-of-function assays. The miRNAs directly targeting E2F3 were identified by bioinformatics analysis and luciferase reporter experiment. Chromatin immunoprecipitation was carried out to reveal the correlation between E2F3 and PLK1.
resultsE2F3 expression was frequently up-regulated in GC tissues, and its high expression might imply poor prognosis. Downregulation of E2F3 restrained GC migration and invasion in vitro and in vivo. Interestingly, we proved that miR-152 was an upstream regulator of E2F3. Moreover, miR-152 reduced E2F3 expression by directly targeting its 3'-UTR, and then modulated GC metastasis via polo-like kinase 1 (PLK1) mediated protein kinase B (AKT) and extracellular signal-regulated kinase (ERK) signals.
conclusionE2F3 plays a crucial role in GC progression and the newly discovered miR-152/E2F3/PLK1 axis provides a new underlying target for therapy of metastasis in GC patients.
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