ArticleOncoTargets and therapy2020
Forkhead Box S1 Inhibits the Progression of Hepatocellular Carcinoma.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 4 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- FOXS1, frequently inactivated by promoter methylation, inhibited colorectal cancer cell growth by promoting TGFBI degradation through autophagy-lysosome pathway.Journal of advanced research · 2025Article
- Transcriptome Profile Reveals Genetic and Metabolic Mechanisms Related to Essential Fatty Acid Content of IntramuscularMetabolites · 2022Article
- Pan-Cancer Analysis Predicts FOXS1 as a Key Target in Prognosis and Tumor Immunotherapy.International journal of general medicine · 2022Article
- FOXS1 Promotes Tumor Progression by Upregulating CXCL8 in Colorectal Cancer.Frontiers in oncology · 2022Article
Corrections and comments
- Retracted
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionForkhead box (FOX) superfamily members were recently shown to play important roles in tumor development and progression. Forkhead box S1 (FOXS1), a member of the FOX family, has been reported to be closely associated with malignant neoplasms. However, its expression and effect on hepatocellular carcinoma remain unclear. The aim of this study was to determine the expression and role of FOXS1 in hepatocellular carcinoma (HCC).
methodsReal-time PCR, Western blot and immunohistochemistry assays were carried out to determine FOXS1 expression in HCC tissues and cells. The biological roles of FOXS1 in HCC were investigated using CCK-8, colony formation, transwell and wound healing. Additionally, the effect of FOXS1 on epithelial-mesenchymal transition (EMT) was investigated by Western blotting. Xenograft model was carried out to evaluate the effect of FOXS1 in vivo.
resultsIn our study, we confirmed lower FOXS1 expression in HCC samples than in normal liver tissues by performing Western blotting, immunohistochemistry and real-time PCR assays. In addition, FOXS1 expression is strongly associated with the prognosis of patients with HCC. Overexpression of FOXS1 suppressed cell proliferation, colony formation, the epithelial-mesenchymal transition (EMT) and the hedgehog (Hh) signaling pathway in vitro and in vivo. SAG, an activator of Hh signaling, partially reversed the effect of FOXS1 overexpression on HCC cells.
conclusionFOXS1 might suppress HCC cell proliferation, colony formation, and EMT by inhibiting the Hh signaling pathway, indicating that FOXS1 may be a promising biological target in HCC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.