ArticleHeliyon2023
CIZ1 aggravates gastric cancer progression via mediating FBXL19-AS1 and miR-339-3p.
Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastric cancer (GC) remains a prevalent malignancy with high morbidity and mortality. CDKN1A interacting zinc finger protein 1 (CIZ1) has been demonstrated to have oncogenic functions in the development of cancers. We detected CIZ1 expression via quantitative real-time PCR (RT-qPCR). The protein level of CIZ1 was measured through Western blot. We noticed that CIZ1 expression was markedly enhanced in GC cells. Furthermore, functional experiments including colony formation assay, EdU staining assay, transwell assay, TUNEL staining assay and flow cytometry analysis uncovered that CIZ1 silencing attenuated cell malignant phenotypes in GC. Through bioinformatics tools and mechanism assays, we explored the up-stream mechanism of CIZ1 and determined that CIZ1 was modulated by FBXL19 antisense RNA 1 (FBXL19-AS1) and microRNA-339-3p (miR-339-3p). Additionally, miR-339-3p exerted a negative role on GC development in vitro, and FBXL19-AS1 depletion also had the inhibitory impacts on the progression of GC in vitro. Eventually, the finding that CIZ1 overexpression reversed the effects of FBXL19-AS1 silencing on GC development was validated by rescue assays. In a word, CIZ1 functioned as a tumor promoter in GC, indicating that CIZ1 might be a promising target for GC treatment.
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