ArticleOncotarget2016
miR-217 and CAGE form feedback loop and regulates the response to anti-cancer drugs through EGFR and HER2.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- The RNA helicase DDX53 (CAGE) contributes to RNA metabolism in a human germ cell model.bioRxiv : the preprint server for biology · 2026Article
- The mechanism of ncRNA in trastuzumab resistance in HER2-positive tumors.Medical oncology (Northwood, London, England) · 2025Review
- miR-429 Suppresses Endometrial Cancer Progression and Drug Resistance via DDX53.Journal of personalized medicine · 2023Article
- DDX43 mRNA expression and protein levels in relation to clinicopathological profile of breast cancer.PloS one · 2023Article
- Potential of the miR-200 Family as a Target for Developing Anti-Cancer Therapeutics.International journal of molecular sciences · 2022Review
- Improving Gemcitabine Sensitivity in Pancreatic Cancer Cells by Restoring miRNA-217 Levels.Biomolecules · 2021Article
- The CAGE-MiR-181b-5p-S1PR1 Axis Regulates Anticancer Drug Resistance and Autophagy in Gastric Cancer Cells.Frontiers in cell and developmental biology · 2021Article
- Histone Deacetylase Inhibitors to Overcome Resistance to Targeted and Immuno Therapy in Metastatic Melanoma.Frontiers in cell and developmental biology · 2020Review
- Review
- Role of HDAC3-miRNA-CAGE Network in Anti-Cancer Drug-Resistance.International journal of molecular sciences · 2018Review
- Potential Regulatory Roles of MicroRNAs and Long Noncoding RNAs in Anticancer Therapies.Molecular therapy. Nucleic acids · 2018Review
- CAGE Binds to Beclin1, Regulates Autophagic Flux and CAGE-Derived Peptide Confers Sensitivity to Anti-cancer Drugs in Non-small Cell Lung Cancer Cells.Frontiers in oncology · 2018Article
- DDX53 Regulates Cancer Stem Cell-Like Properties by Binding to SOX-2.Molecules and cells · 2017Article
- DDX53 Promotes Cancer Stem Cell-Like Properties and Autophagy.Molecules and cells · 2017Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA array analysis revealed that miR-217 expression was decreased in anti-cancer drug-resistant Malme3MR cancer cells. CAGE, a cancer/testis antigen, was predicted as a target of miR-217. Luciferase activity and ChIP assays revealed a negative feedback relationship between CAGE and miR-217. miR-217 and CAGE oppositely regulated the response to anti-cancer drugs such as taxol, gefitinib and trastuzumab, an inhibitor of HER2. miR-217 negatively regulated the tumorigenic, metastatic, angiogenic, migration and invasion potential of cancer cells. The xenograft of Malme3MR cells showed an increased expression of pEGFRY845. CAGE and miR-217 inhibitor regulated the expression of pEGFRY845. CAGE showed interactions with EGFR and HER2 and regulated the in vivo sensitivity to trastuzumab. The down-regulation of EGFR or HER2 enhanced the sensitivity to anti-cancer drugs. CAGE showed direct regulation of HER2 and was necessary for the interaction between EGFR and HER2 in Malme3MR cells. miR-217 inhibitor induced interactions of CAGE with EGFR and HER2 in Malme3M cells. The inhibition of EGFR by CAGE-binding GTGKT peptide enhanced the sensitivity to gefitinib and trastuzumab and prevented interactions of EGFR with CAGE and HER2. Our results show that miR-217-CAGE feedback loop serves as a target for overcoming resistance to various anti-cancer drugs, including EGFR and HER2 inhibitors.
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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.