ArticleOncology reports2019
Targeting the differentiation of gastric cancer cells (KATO‑III) downregulates epithelial‑mesenchymal and cancer stem cell markers.
Article in Oncology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Advances in protein microarray-based proteomics for gastric cancer applications in biomarker discovery, molecular subtyping, and precision oncology.Frontiers in oncology · 2026Review
- TGF-β Receptor Inhibitor SB431542 Enhanced the Sensitivity of Gastric Cancer to 5-Fluorouracil: New Combined Targeted Therapy.International journal of molecular sciences · 2025Article
- The plasticity of epithelial cells and its potential in the induced differentiation of gastric cancer.Cell death discovery · 2024Review
- Optimization ofInternational journal of molecular sciences · 2024Article
- Developing New Peptides and Peptide-Drug Conjugates for Targeting the FGFR2 Receptor-Expressing Tumor Cells and 3D Spheroids.Biomimetics (Basel, Switzerland) · 2024Article
- Article
- Integrated regulation of chondrogenic differentiation in mesenchymal stem cells and differentiation of cancer cells.Cancer cell international · 2022Review
- Hyaluronic AcidCartilage · 2021Article
- Transcriptional and Epigenetic Bioinformatic Analysis of Claudin-9 Regulation in Gastric Cancer.Journal of oncology · 2021Article
- TNF‑α promotes the malignant transformation of intestinal stem cells through the NF‑κB and Wnt/β‑catenin signaling pathways.Oncology reports · 2020Article
- Differentiation of cancer cells upregulates HLA‑G and PD‑L1.Oncology reports · 2020Article
- Promotion of miR-221-5p on the Sensitivity of Gastric Cancer Cells to Cisplatin and Its Effects on Cell Proliferation and Apoptosis by Regulating DDR1.OncoTargets and therapy · 2020Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to analyze the acquisition of the differentiated phenotype in the human gastric signet ring cell adenoma cancer KATO‑III cell line in vitro. The morphology of KATO‑III cells was explored by microcinematography. Different cytokines secreted by both adherent and non‑adherent KATO‑III cells into medium were observed. The cancer stem cell phenotypes were identified by reverse transcription‑quantitative polymerase chain reaction using primers (E‑Cad, Slug, Snail, vimentin, NANOG, NESTIN, OCT3/4 and C‑X‑C motif chemokine receptor 4) or antibodies [cluster of differentiation (CD)90 and CD117] by flow cytometry (FACS). The influence of the induction media for the differentiation of mesenchymal cells was studied through viability and proliferation assays, by evaluating gene expression and the expression of markers via FACS. Cell viability and cell cycle distribution were evaluated following the treatment of KATO‑III with acetyl salicylic acid and using the induction media as an inhibitor of epithelial‑mesenchymal transition (EMT) and heparanase. A total of 3 phenotypes of KATO‑III were observed (adherent, non‑adherent and cell cluster), which have internal potential for cell transition into one of the other phenotypes. KATO‑III was differentiated into adipocyte‑, chondrocyte‑, osteocyte‑ and neurocyte‑like cells by the induction media. Identification of the induced cells was conducted using cell dyes. Reduced mRNA expression of EMT‑associated molecules, stem cell markers and heparanase was observed with acetyl salicylic acid and induction media. An inhibitory effect of acetyl salicylic acid and the induction media was also noted in regard to cell proliferation. In addition, acetyl salicylic acid induced G0/G1 phase cell cycle arrest in KATO‑III cells. In conclusion, the induction of the differentiation of cancer stem cells into non‑proliferating cells offers the possibility for novel drug design to overcome the issues associated with metastasis, drug resistance and systemic toxicity with improved therapeutic efficacy.
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