ArticleMolecular medicine reports2018
ASCL2 expression contributes to gastric tumor migration and invasion by downregulating miR223 and inducing EMT.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Combined EP300 and CREBBP Expression Levels Regulate Human Trophoblast Differentiation.International journal of molecular sciences · 2026Article
- ASCL2 drives colorectal cancer metastasis through transcriptional activation of TDGF1.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- ASCL2 contributes to clinical assessments of breast cancer and mediates tumor progression via the interaction with CLDN3.Scientific reports · 2025Article
- Unravelling NK cell subset dynamics and specific gene signatures post-ibrutinib therapy in chronic lymphocytic leukaemia via single-cell transcriptomics.BMC cancer · 2025Article
- The histone acetylation-related gene signature predicts prognosis and immunotherapy response in stomach adenocarcinoma.Frontiers in oncology · 2025Article
- Achaete-scute family bHLH transcription factor 2 activation promotes hepatoblastoma progression.Cancer science · 2024Article
- Article
- EP300 facilitates human trophoblast stem cell differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Identification and Validation of a m5C RNA Modification-Related Gene Signature for Predicting Prognosis and Immunotherapeutic Efficiency of Gastric Cancer.Journal of oncology · 2023Article
- Epithelial to Mesenchymal Transition: A Challenging Playground for Translational Research. Current Models and Focus onInternational journal of molecular sciences · 2021Review
- Introducing the Stem Cell ASCL2 Reporter STAR into Intestinal Organoids.STAR protocols · 2020Article
- Phylogenetic analysis of achaete-scute complex genes in metazoans.Molecular genetics and genomics : MGG · 2020Article
- Serum levels of miR-223 but not miR-21 are decreased in patients with neuroendocrine tumors.PloS one · 2020Observational
- Overexpression of E74-Like Factor 5 (ELF5) Inhibits Migration and Invasion of Ovarian Cancer Cells.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Knockdown of BRCC3 exerts an anti‑tumor effect on cervical cancer in vitro.Molecular medicine reports · 2018Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Achaete‑scute homolog 2 (ASCL2), a basic helix‑loop‑helix transcription factor, serves an essential role in the maintenance of adult intestinal stem cells and the growth of gastric cancer (GC). However, the function of ASCL2 in the metastasis of GC is poorly understood. The present study aimed to evaluate the effect of ASCL2 expression on gastric tumor metastasis. ASCL2 protein expression was detected in 32 cases of gastric metastasis and its relevant primary tumors using western blotting and immunohistochemistry. The data suggested that the expression of ASCL2 was highest in metastatic tumors, among adjacent normal tissues, primary gastric tumors and gastric metastatic tumors. Furthermore, ASCL2‑overexpressing GC cell lines MKN1‑ASCL2 and SNU16‑ASCL2 were established. An in vitro assay suggested that microRNA 223 (miR223) expression was downregulated following ASCL2 overexpression, and that the expression of the epithelium‑associated protein E‑cadherin was significantly decreased, while a series of mesenchyme‑associated proteins, including zinc finger E‑box‑binding homeobox 1 (Zeb‑1), twist‑related protein 1, integrin, vimentin, 72 kDa type IV collagenase and matrix metalloproteinase‑9 were upregulated in ASCL2‑overexpressing cells. Overexpression of miR223 attenuated the epithelial‑mesenchymal transition (EMT)‑promoting effect induced by ASCL2 expression. In addition, the results of the chromatin immunoprecipitation and luciferase reporter gene assays indicated that ASCL2 was able to interact with the promoter of pre‑miR223, and to inhibit the maturation of miR223, which may interact with the 3' untranslated region of Zeb‑1 and inhibit EMT in tumor cells. The results of the present study demonstrated that ASCL2 was able to downregulate the expression level of miR223, contribute to EMT and promote gastric tumor metastasis, which indicated that ASCL2 may serve as a therapeutic target in the treatment of GC.
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