ArticleInternational journal of nanomedicine2021
Exosomal miR-136-5p Derived from Anlotinib-Resistant NSCLC Cells Confers Anlotinib Resistance in Non-Small Cell Lung Cancer Through Targeting PPP2R2A.
Article in International journal of nanomedicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 36 citations in OpenAlex.
- Multiomics profiling and experiments in preclinical models revealed RAD51-IN-1 as a synergistic potentiator of anlotinib sensitivity.Science advances · 2026Trial
- Breaking senescence restriction: MAFK-AREG axis promotes NSCLC cells to resist doxorubicin.Oncology letters · 2026Article
- Expression of urinary exosomal miR-136-5p in diabetic kidney disease and evaluation of its clinical diagnostic value.Scientific reports · 2025Article
- Exosome-Mediated Chemoresistance in Cancers: Mechanisms, Therapeutic Implications, and Future Directions.Biomolecules · 2025Review
- Synergizing Success: The Role of Anlotinib Combinations in Advanced Non-Small Cell Lung Cancer Treatment.Pharmaceuticals (Basel, Switzerland) · 2025Review
- RAF1 promotes anlotinib resistance in non-small cell lung cancer by inhibiting apoptosis.Journal of cancer research and clinical oncology · 2025Article
- Off-label use of anlotinib in malignancies' treatment: efficacy and management of adverse reactions.Pharmacological reports : PR · 2025Review
- Intratumoral heterogeneity and drug resistance in cancer.Cancer cell international · 2025Review
- NClinical and translational medicine · 2025Article
- Extracellular Vesicles as Mediators and Potential Targets in Combating Cancer Drug Resistance.Molecules (Basel, Switzerland) · 2025Review
- Molecular Mechanisms and Roles of MiR-136-5p in Human Cancer and Other Disorders.Current medicinal chemistry · 2025Review
- Astragaloside IV Overcomes Anlotinib Resistance in Non-small Cell Lung Cancer through miR-181a-3p/UPR-ERAD Axis.Current computer-aided drug design · 2025Article
- Research and progress of microRNA-136 in metastatic tumors.Frontiers in oncology · 2025Review
- Functional tumor-derived exosomes in NSCLC progression and clinical implications.Frontiers in pharmacology · 2025Review
- Harnessing EVs-ncRNA for Lung Cancer: From Oncogenic Pathways to Novel Diagnostic and Therapeutic Strategies.International journal of nanomedicine · 2025Review
- Recent advances to address challenges in extracellular vesicle-based applications for lung cancer.Acta pharmaceutica Sinica. B · 2024Review
- Unraveling the Connection: Extracellular Vesicles and Non-Small Cell Lung Cancer.International journal of nanomedicine · 2024Review
- Composition of Conditioned Media from Radioresistant and Chemoresistant Cancer Cells Reveals miRNA and Other Secretory Factors Implicated in the Development of Resistance.International journal of molecular sciences · 2023Review
- The therapeutic potential of exosomes in lung cancer.Cellular oncology (Dordrecht, Netherlands) · 2023Review
- PVT1/miR-136/Sox2/UPF1 axis regulates the malignant phenotypes of endometrial cancer stem cells.Cell death & disease · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAnlotinib resistance is a challenge for advanced non-small cell lung cancer (NSCLC). Understanding the underlying mechanisms against anlotinib resistance is of great importance to improve prognosis and treatment of patients with advanced NSCLC.
methodsRT-qPCR assay was used to assess the level of miR-136-5p in anlotinib-resistant NSCLC cells and exosomes derived from anlotinib-resistant NSCLC cells. In addition, miR-136-5p level in tumor tissues from patients who exhibited a poor response to anlotinib therapy and patients who were therapy naïve or patients who exhibited a positive response to anlotinib therapy was detected by RT-qPCR assay.
resultsIn this study, we found that high levels of plasma exosomal miR-136-5p is correlated with clinically poor anlotinib response. In addition, anlotinib-resistant NSCLC cells promoted parental NSCLC cell proliferation via transferring functional miR-136-5p from anlotinib-resistant NSCLC cells to parental NSCLC cells via exosomes. Moreover, exosomal miR-136-5p could endow NSCLC cells with anlotinib resistance by targeting PPP2R2A, leading to the activation of Akt pathway. Furthermore, miR-136-5p antagomir packaging into anlotinib-resistant NSCLC cell-derived exosomes functionally restored NSCLC cell anlotinib sensitivity in vitro. Animal studies showed that A549/anlotinib cell-derived exosomal miR-136-5p agomir promoted A549 cell anlotinib resistance in vivo.
conclusionCollectively, these findings indicated that anlotinib-resistant NSCLC cell-derived exosomal miR-136-5p confers anlotinib resistance in NSCLC cells by targeting PPP2R2A, indicating miR-136-5p may act as a potential biomarker for anlotinib response in NSCLC.
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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.