ArticleInternational journal of general medicine2024
MiR-21-5p Modulates Cisplatin-Resistance of CD44+ Gastric Cancer Stem Cells Through Regulating the TGF-β2/SMAD Signaling Pathway.
Article in International journal of general medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Mechanisms of chemoresistance in gastric cancer: interplay between microRNAs and the tumor microenvironment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Role of microRNAs in cisplatin response of cancer stem cells.Stem cell research & therapy · 2026Review
- Correlation of serum exosomal miR-21 with the risk of gastric cancer onset: its value for early diagnosis.American journal of translational research · 2026Article
- Stemness signatures reflect prognostic disturbances in gastric cancer.World journal of gastrointestinal oncology · 2025Article
- Hotspots and trends in gastric cancer stem cell research: a visualization and bibliometric analysis.Frontiers in oncology · 2025Review
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Authors and funding
11 authors.
Funding
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Abstract
Background: Cisplatin (DDP) resistance in gastric cancer (GC) is likely to come from gastric cancer stem cells (GCSC). It is a new idea to study the mechanism of the DDP-resistance in GCSC from miRNA. Materials and Methods: CD44+ GCSCs and CD44- control cells were constructed based on the HGC27 gastric cancer cell line. DDP sensitivities in CD44+ and CD44- cells were detected via CCK-8 assay. The differential expression of miR-21-5p in these cell lines was detected by RT‒qPCR. The expression levels of downstream TGF-β2, SMAD2 and SMAD3 were determined through RT‒PCR and Western blotting. A luciferase assay was used to detect the relationship between miR-21-5p and TGFB2, and the TCGA database, clinical data from our centre, and vivo experiment were used for validation. Finally, we knocked down miR-21-5p to detect changes in cisplatin resistance in GCSCs and to verify changes in the levels of downstream pathways in GCSCs. Results: CD44+ GCSCs induced cisplatin resistance compared with CD44- cells. miR-21-5p was highly expressed in GCSCs, and the TGF-β2/SMAD pathway was also highly expressed. TGFB2 was proven to be a downstream target gene of miR-21-5p and had a positive relationship with it in phenotype. After knockdown of miR-21-5p, the TGF-β2/SMAD pathway was also inhibited, and the resistance of GCSCs to cisplatin was specifically decreased. Conclusion: MiR-21-5p promotes cisplatin resistance in gastric cancer stem cells by regulating the TGF-β2/SMAD signalling pathway.
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