ArticleNon-coding RNA research2024
A dynamic Boolean network reveals that the BMI1 and MALAT1 axis is associated with drug resistance by limiting miR-145-5p in non-small cell lung cancer.
Article in Non-coding RNA research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 27 citations in OpenAlex.
- A stress granule-associated RNA-binding protein FAM120A drives cisplatin resistance in non-small cell lung cancer.Journal of biochemistry · 2026Article
- RNA sequencing reveals differential expression of circular RNAs in human small cell lung cancer.Scientific reports · 2026Article
- Research progress of MicroRNA in lung cancer.Discover oncology · 2026Review
- p53 Orchestrates the Immunogenic-Tolerogenic Pyroptosis Switch in Non-Small Cell Lung Cancer: A Systems Biology Approach.Computational and structural biotechnology journal · 2026Article
- Lung Cancer Chemoresistance: Insights into the Regulatory Role of lncRNAs.Cancer management and research · 2026Review
- Boolean-network simplification and rule fitting to unravel chemotherapy resistance in non-small cell lung cancer.PloS one · 2026Article
- MALAT1 as a molecular driver of tumor progression, immune evasion, and resistance to therapy.Molecular cancer · 2025Review
- Targeting the FOXA1/BMI1 axis to overcome chemoresistance and suppress tumor progression in nasopharyngeal carcinoma.Cell death discovery · 2025Article
- Targeting NSCLC drug resistance: Systems biology insights into the MALAT1/miR-145-5p axis and Wip1 in regulating ferroptosis and apoptosis.Journal of the Royal Society, Interface · 2025Article
- [Epithelial-mesenchymal Transition: Biological Basis and Clinical Prospects of Lung Cancer Invasion, Metastasis, and Drug Resistance].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2025Review
- LncRNA ZEB1-AS1 promotes the proliferation and migration of non-small cell lung cancer by activating epithelial-mesenchymal transition with STAT3.Translational cancer research · 2025Article
- Engineered exosomes: a promising design platform for overcoming cancer therapy resistance.Frontiers in cell and developmental biology · 2025Review
- Has_circ_0002360 promotes the progression of lung adenocarcinoma by activating miR-762 and regulating PODXL expression.Translational cancer research · 2024Article
- LncRNA PTENP1/miR-21/PTEN Axis Modulates EMT and Drug Resistance in Cancer: Dynamic Boolean Modeling for Cell Fates in DNA Damage Response.International journal of molecular sciences · 2024Article
- Exosomal microRNAs in lung cancer: a narrative review.Translational cancer research · 2024Review
- A risk score based on polyamine metabolism and chemotherapy-related genes predicts prognosis and immune cells infiltration of lung adenocarcinoma.Journal of cellular and molecular medicine · 2024Article
- LINC01559 promotes lung adenocarcinoma metastasis by disrupting the ubiquitination of vimentin.Biomarker research · 2024Article
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6 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Patients with non-small cell lung cancer (NSCLC) are often treated with chemotherapy. Poor clinical response and the onset of chemoresistance limit the anti-tumor benefits of drugs such as cisplatin. According to recent research, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA related to cisplatin resistance in NSCLC. Furthermore, MALAT1 targets microRNA-145-5p (miR-145), which activates Krüppel-like factor 4 (KLF4) in associated cell lines. B lymphoma Mo-MLV insertion region 1 homolog (BMI1), on the other hand, inhibits miR-145 expression, which stimulates Specificity protein 1 (Sp1) to trigger the epithelial-mesenchymal transition (EMT) process in pemetrexed-resistant NSCLC cells. The interplay between these molecules in drug resistance is still unclear. Therefore, we propose a dynamic Boolean network that can encapsulate the complexity of these drug-resistant molecules. Using published clinical data for gain or loss-of-function perturbations, our network demonstrates reasonable agreement with experimental observations. We identify four new positive circuits: miR-145/Sp1/MALAT1, BMI1/miR-145/Myc, KLF4/p53/miR-145, and miR-145/Wip1/p38MAPK/p53. Notably, miR-145 emerges as a central player in these regulatory circuits, underscoring its pivotal role in NSCLC drug resistance. Our circuit perturbation analysis further emphasizes the critical involvement of these new circuits in drug resistance for NSCLC. In conclusion, targeting MALAT1 and BMI1 holds promise for overcoming drug resistance, while activating miR-145 represents a potential strategy to significantly reduce drug resistance in NSCLC.
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