ArticleTranslational cancer research2020
The miR-567/RPL15/TGF-β/Smad axis inhibits the stem-like properties and chemo-resistance of gastric cancer cells.
Article in Translational cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Role of microRNAs in cisplatin response of cancer stem cells.Stem cell research & therapy · 2026Review
- miR-567 indicates atherosclerosis development and regulates inflammation, phenotype switch, proliferation, and migration of platelet-derived growth factor (PDGF)-BB-induced vascular smooth muscle cells (VSMCs) via CSF1R.Journal of molecular histology · 2026Article
- Signaling pathways as the pivotal regulators of cisplatin resistance in tumor cells through SOX2 upregulation.Medical oncology (Northwood, London, England) · 2025Review
- Clinical significances ofBiomedical reports · 2025Article
- Non-Coding RNA as Biomarkers and Their Role in the Pathogenesis of Gastric Cancer-A Narrative Review.International journal of molecular sciences · 2024Review
- Prognostic evaluation of pancreatic cancer based on the model of chemo-radiotherapy resistance-related genes.Journal of gastrointestinal oncology · 2023Article
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5 authors at 1 institution in 1 country.
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Abstract
backgroundGastric cancer (GC) is the second most significant contributor to cancer-related mortality in China. GC treatment is often hindered by metastasis and chemoresistance, which leads to poor prognosis. This study set out to investigate the role of miR-567 on the stem-like properties and chemo-resistance of GC cells, as well as its potential molecular mechanism.
methodsThe expression of miR-567 in GES-1, AGS, SCG-7901, MGC-803, SUN-16, and MKN1 cell lines was detected by Real-time PCR. AGS cells were transfected with NC or miR-567 mimics and RPL15 3'UTR (wt) or RPL15 3'UTR (mut) using Lipofectamine 2000. CCK-8, 5-ethynyl-2'-deoxyuridine (EdU) assay were detected the effect of miR-567/RPL15/TGF-β/Smad on gastric cancer cell viability and proliferation, respectively. Western blot were used to analyze the effects of miR-567/RPL15/TGF-β/Smad on protein levels of SOX2, NANOG, ALDH1A1, TGF-β1, TGFβ-R1, SMAD1, P-SMAD1, SMAD2 and P-SMAD2.
resultsThe results showed that the expression of miR-567 was down-regulated in GC cell lines. TargetScan and luciferase report assay indicated that RPL15 was the target of miR-567. Functional analysis discovered that the overexpression of miR-567 inhibited the microsphere formation of AGS stem cells, while PRL15 overexpression promoted the formation of microspheres in AGS cells. Through Western blot analysis, miR-567 overexpression was further revealed to inhibit the expression of stem-like marker proteins (SOX2, NANOG, and ALDH1A1). Furthermore, PRL15 overexpression was found to significantly promote the growth of AGS/DDP cells, while miR-567 overexpression reversed the effect of PRL15 on cisplatin-resistant cell growth. The relationship between miR-567 and the TGF-β1/TGFβ-R1/Smad2/Smad3 pathway was also shown. The addition of TGF-β/Smad pathway inhibitor LY 3200882 significantly inhibited the expression of PRL-15, TGF-β1, TGF-R1, p-Smad1, and p-sSmad2, while reversing the effect of miR-567 inhibitor on stem-like properties and chemical resistance.
conclusionsFinally, this study elucidated the effect of miR-567 on the stem-like properties and chemical resistance of GC cells via the RPL15 /TGF-beta/Smad axis.
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