ArticleAmerican journal of translational research2021
Effect of miR-133b on progression and cisplatin resistance of triple-negative breast cancer through FGFR1-Wnt-β-catenin axis.
Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The trial behind it
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- MIR133B-SEPT9 axis suppresses colorectal cancer progression by inhibiting β-catenin-mediated EMT signaling and is associated with poor prognosis.Molecular medicine (Cambridge, Mass.) · 2026Article
- miR-96-5p antagonizes FOXQ1-driven WNT/β-catenin signaling to inhibit triple-negative breast cancer.Scientific reports · 2026Article
- β-catenin as a key regulator of the cisplatin response in tumor cells.Clinical and experimental medicine · 2025Review
- Advances in the Understanding of the Pathogenesis of Triple-Negative Breast Cancer.Cancer medicine · 2024Review
- Oncogenic miR-106b-5p promotes cisplatin resistance in triple-negative breast cancer by targeting GDF11.Histology and histopathology · 2024Article
- Circ_0072088 promotes breast carcinoma progression via modulating miR-607/RNF2 axis.American journal of translational research · 2024Article
- Review
- The Role of MicroRNAs in Breast Cancer and the Challenges of Their Clinical Application.Diagnostics (Basel, Switzerland) · 2023Review
- Breast cancer: miRNAs monitoring chemoresistance and systemic therapy.Frontiers in oncology · 2023Review
- Regulatory role of miRNAs in Wnt signaling pathway linked with cardiovascular diseases.Current research in pharmacology and drug discovery · 2022Article
- MicroRNA Expression Profiles and Breast Cancer Chemotherapy.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAs a type of breast cancer that has relatively strong invasiveness, triple negative breast cancer (TNBC) seriously affects the survival of patients. microRNAs (miRNAs) have been shown to exert a prominent regulatory effect on the disease, among which miR-133b is reported to be involved in the pathological mechanism of breast cancer, but its role in TNBC remains unclear.
methodsIn this study, real-time quantitative PCR (RT-qPCR) and Western blotting (WB) were performed for detecting the expressions of miR-133b, fibroblast growth factor receptor 1 (FGFR1), and Wingless/Integrated (Wnt)-β-catenin pathway markers (Wnt1, β-catenin, nuclear-β-catenin, p-GSK-3β, GSK-3β, cyclinD1, and FOXQ1). With TNBC cells and DDP-resistant TNBC cells (TNBC/DDP cells) used as research objects, their proliferation and apoptosis were measured by Cell Counting Kit-8 (CCK-8) assays and Flow cytometry, respectively. Then, the targeted relationship between miR-133b and FGFR1 was verified by Dual luciferase reporter gene assay (DLRGA).
resultsIn our study, miR-133b was down-regulated while FGFR1 up-regulated in TNBC. The ectopic expression of miR-133b remarkably inhibited the proliferation and colony formation but induced apoptosis of TNBC cells, and inactivated the Wnt-β-catenin pathway. The knockdown of FGFR1 had similar effects. Additionally, miR-133b targeted and negatively regulated FGFR1. Up-regulating miR-133b or down-regulating FGFR1 could enhance the proliferation and DDP sensitivity of TNBC cells or TNBC/DDP cells. Up-regulating FGFR1 could offset the anti-TNBC cell survival and DDP sensitization shown by ectopic expression of miR-133b.
conclusionTo sum up, miR-133b can inhibit the growth and DDP resistance of TNBC cells by targeting FGFR1 and inactivating the Wnt-β-catenin pathway.
Indexed as
Identifiers
34306338PMC8290659W3185118500What OpenQuestion holds
Registered trials
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.