ArticleScientific reports2022
METTL3/LINC00662/miR-186-5p feedback loop regulates docetaxel resistance in triple negative breast cancer.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 24 citations in OpenAlex.
- Integrating circulating microRNAs with epidemiological factors enhances breast cancer detection across subtypes: the MCC-Spain study.Scientific reports · 2026Article
- Targeting intracellular mRNA mJournal of advanced research · 2026Review
- Mapping Non-Coding Epimutations in Breast Cancer: Advancing Epigenetics Towards Precision Medicine.Sub-cellular biochemistry · 2026Review
- Enhanced multi-omics analysis reveals a lncRNA signature with 12 RNA modifications to predict tumor heterogeneity and potential therapy in non-small cell lung cancer.Discover oncology · 2025Article
- Prognostic value of Linc00662/miR-16-5p/FASN in cervical cancer and regulation of tumor progression.Hereditas · 2025Article
- Potential regulatory role of the mActa biochimica et biophysica Sinica · 2025Review
- Docetaxel Resistance in Breast Cancer: Current Insights and Future Directions.International journal of molecular sciences · 2025Review
- Role of M2 macrophage-derived exosomes in cancer drug resistance via noncoding RNAs.Discover oncology · 2025Review
- Diagnostic Value of Glycosylated Extracellular Vesicle microRNAs in Gastric Cancer.Cancer management and research · 2025Article
- Advances in the Understanding of the Pathogenesis of Triple-Negative Breast Cancer.Cancer medicine · 2024Review
- The lncRNA AFAP1-AS1 is upregulated in metastatic triple-negative breast tumors and controls hypoxia-activated vasculogenic mimicry and angiogenesis.BMC cancer · 2024Article
- Functions of methyltransferase-like 3 in breast cancer: pathogenesis, drug resistance, and therapeutic target.Breast cancer research : BCR · 2024Review
- Identification of necroptosis-related genes in ankylosing spondylitis by bioinformatics and experimental validation.Journal of cellular and molecular medicine · 2024Article
- LINC01806 Promotes Breast Cancer Growth and Metastasis via Sponging miR-1286 to Disinhibit ZEB1 Expression.Biochemical genetics · 2024Article
- Small molecule inhibitors targeting mJournal of hematology & oncology · 2024Review
- Targeting RNA modifications with pharmacological agents: New frontiers in cancer therapy.Cancer medicine · 2024Review
- Non-coding RNA-Mediated N6-Methyladenosine (mNon-coding RNA research · 2024Review
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- Super Carbonate Apatite-miR-497a-5p Complex Is a Promising Therapeutic Option against Inflammatory Bowel Disease.Pharmaceuticals (Basel, Switzerland) · 2023Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insight into the mechanism of docetaxel resistance in breast cancer may help to improve prognosis. We aimed to investigate the role of N6-methyladenosine (m6A) and the METTL3/LINC00662/miR-186-5p pathway in regulating docetaxel resistance in triple negative breast cancer (TNBC). We have recruited 193 pathologically diagnosed TNBC patients from 2016 to 2017 in our hospital. Quantitative real-time PCR was used to evaluate the expression of LINC00662 and miR-186-5p both in vivo and in vitro. CCK8 tests were used to assess cell viability. ELISA was used for protein expression evaluation. Dual luciferase reporter gene assay and RNA pull-down were used to evaluate the interaction between LINC00662 and miR-186-5p. m6A levels were enhanced in breast cancer tissues and cells. LINC00662, miR-186-5p and METTL3 were differentially expressed in vivo, and METTL3 expression was associated with LINC00662 and miR-186-5p expression. LINC00662 and miR-186-5p were differentially expressed in vitro; LINC00662 promoted cell viability and decreased the apoptosis rate, whereas miR-186-5p inhibited cell viability and increased the apoptosis rate. Furthermore, we found that METTL3 regulated m6A levels in docetaxel-resistant breast cancer cells by regulating the expression of LINC00662. Moreover, LINC00662 and miR-186-5p regulated the cell viability rate of docetaxel-resistant breast cancer cells. Further experiments showed that LINC00662 directly interacted with miR-186-5p to exert biological functions; besides miR-186-5p could regulate the expression of METTL3. METTL3 promotes m6A levels and docetaxel resistance in breast cancer by regulating the expression of LINC00662 and miR-186-5p; more experiments are needed to clarify the role of m6A regulation in drug resistance.
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