ArticleInternational journal of clinical and experimental pathology2020
ATOH8 overexpression inhibits the tumor progression and monocyte chemotaxis in hepatocellular carcinoma.
Article in International journal of clinical and experimental pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Loss of Atoh8 Impairs Macroautophagy.Cells · 2025Article
- RNA-seq analysis reveals transcriptome changes in livers fromBiochemistry and biophysics reports · 2025Article
- FXR1 associates with and degrades PDZK1IP1 and ATOH8 mRNAs and promotes esophageal cancer progression.Biology direct · 2024Article
- Long-term severe hypoxia adaptation induces non-canonical EMT and a novel Wilms Tumor 1 (WT1) isoform.Cancer gene therapy · 2024Article
- A spatiotemporal atlas of cholestatic injury and repair in mice.Nature genetics · 2024Article
- Upregulation of CELSR1 expression promotes ovarian cancer cell proliferation, migration, and invasion.Medical oncology (Northwood, London, England) · 2023Article
- ATOH8 promotes HBV immune tolerance by inhibiting the pyroptotic pathway in hepatocytes.Molecular medicine reports · 2023Article
- Bioinformatics Analysis of mRNAs and miRNAs for Identifying Potential Biomarkers in Lung Adenosquamous Carcinoma.Computational and mathematical methods in medicine · 2022Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveATOH8 is reported to be associated with the progression of many tumors; however, there are remaining controversies. The aim of this study is to explore the role of ATOH8 in hepatocellular carcinoma (HCC) and its effect on monocyte chemotaxis.
methodsBioinformatics analysis was performed based on the LIHC data in GEPIA and LinkedOmic. Fresh human liver cancer and adjacent nontumor tissue specimens were collected at the Shanghai Public Health Clinical Center. qRT-PCR was performed to determine the transcript level, and western blot analysis and ELISA were used to detect protein expression. CCK8, colony formation, wound-healing, Transwell migration and invasion assays were performed to examine cell proliferation, migration and invasion. An HCC xenograft mouse model was used to determine oncogenicity in vivo. Cell apoptosis and related markers were detected by flow cytometry. Additionally, chemotaxis was assessed by the Transwell migration assay.
resultsATOH8 expression is downregulated in HCC tissue and hepatoma cell lines. High expression of ATOH8 predicts a favorable prognosis. Overexpression of ATOH8 in liver cancer cells inhibits proliferation, migration and invasion in vitro, and tumor progression in nude mice. Knockdown of ATOH8 promotes proliferation of Huh7 and EMT-related proteins. Overexpression of ATOH8 increases chemosensitivity to 5-FU, which is probably caused by inhibiting the phosphorylation of AKT (Ser473). Furthermore, overexpression of ATOH8 in Huh7 reduced MCP1 to inhibit chemotactic THP-1, and promoted antitumor inflammatory cytokine (TNF-α and IFN-γ) secretion in monocytes.
conclusionIn addition to the intrinsic oncosuppressive function of ATOH8 in the liver, ATOH8 may modulate the microenvironment to create an immune activation state. This may partly be attributed to ATOH8 inhibition of the monocyte recruitment via suppressing MCP1 expression so as to promote antitumor inflammatory cytokine secretion in monocytes.
Indexed as
Identifiers
33165366PMC7642694W3106290358What OpenQuestion holds
Registered trials
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.