ArticleJournal of cellular and molecular medicine2019
Trans-3,5,4´-trimethoxystilbene reduced gefitinib resistance in NSCLCs via suppressing MAPK/Akt/Bcl-2 pathway by upregulation of miR-345 and miR-498.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Structural Modification of Resveratrol: Biological Activities and Anticancer Potential of Emerging Methoxylated Analogs.International journal of molecular sciences · 2026Review
- Early radiotherapy delays acquired gefitinib resistance in EGFR-mutant NSCLC by suppressing c-FOS-associated survival signaling.Respiratory research · 2026Article
- Natural compounds for non-small cell lung cancer treatment: focus on the EGFR signaling pathway.Frontiers in pharmacology · 2026Review
- An Overview of Targeting Some Cancer Hallmarks with Plant Polyphenols: A Step Toward Precision.Sub-cellular biochemistry · 2026Review
- Dual Disruption of EGFR/PI3K Signaling: IGF2BP2 Targeting Reverses Anti-EGFR Resistance in CAFs-Infiltrated Oral Squamous Cell Carcinoma.International journal of molecular sciences · 2025Article
- MicroRNAs as Sensitizers of Tyrosine Kinase Inhibitor Resistance in Cancer: Small Molecule Partnerships.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Aidi injection inhibits the migration and invasion of gefitinib-resistant lung adenocarcinoma cells by regulating the PLAT/FAK/AKT pathway.Chinese medicine · 2025Article
- M6A RNA modification: focusing on non-small cell lung cancer progression, therapeutic strategies and challenges.Frontiers in oncology · 2025Review
- Advances in antitumor effects of pterostilbene and its derivatives.Future medicinal chemistry · 2025Review
- Hippo pathway in non-small cell lung cancer: mechanisms, potential targets, and biomarkers.Cancer gene therapy · 2024Review
- The Underlying Mechanism Involved in Gefitinib Resistance and Corresponding Experiment Validation in Lung Cancer.Mediators of inflammation · 2023Article
- Review
- Polyphenols as Lung Cancer Chemopreventive Agents by Targeting microRNAs.Molecules (Basel, Switzerland) · 2022Review
- Bax/Bcl-2 Cascade Is Regulated by the EGFR Pathway: Therapeutic Targeting of Non-Small Cell Lung Cancer.Frontiers in oncology · 2022Review
- Emerging Role of miR-345 and Its Effective Delivery as a Potential Therapeutic Candidate in Pancreatic Cancer and Other Cancers.Pharmaceutics · 2021Review
- Antiparasitic Effect of Stilbene and Terphenyl Compounds againstPharmaceuticals (Basel, Switzerland) · 2021Article
- Knockdown of MIR9‑3HG inhibits proliferation and promotes apoptosis of cervical cancer cells by miR‑498 via EP300.Molecular medicine reports · 2021Article
- Inhibition of Bcl-2 and Bcl-xL overcomes the resistance to the third-generation EGFR tyrosine kinase inhibitor osimertinib in non-small cell lung cancer.Molecular medicine reports · 2021Article
- Combined Treatment of Cinobufotalin and Gefitinib Exhibits Potent Efficacy against Lung Cancer.Evidence-based complementary and alternative medicine : eCAM · 2021Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite initial dramatic efficacy of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (EGFR-TKIs) in EGFR-mutant lung cancer patients, subsequent emergence of acquired resistance is almost inevitable. Resveratrol and its derivatives have been found to exert some effects on EGFR-TKI resistance in non-small cell lung cancer (NSCLC), but the underlying mechanisms remain unclear. We screened several NSCLC cell lines with gefitinib resistance by MTT assay and analysed the miR-345/miR-498 expression levels. NSCLC cells were pre-treated with a resveratrol derivative, trans-3,5,4-trimethoxystilbene (TMS) and subsequently challenged with gefitinib treatment. The changes in apoptosis and miR-345/miR-498 expression were analysed by flow cytometry and q-PCR respectively. The functions of miR-345/miR-498 were verified by CCK-8 assay, cell cycle analysis, dual-luciferase reporter gene assay and immunoblotting analysis. Our results showed that the expression of miR-345 and miR-498 significantly decreased in gefitinib resistant NSCLC cells. TMS pre-treatment significantly upregulated the expression of miR-345 and miR-498 increasing the sensitivity of NSCLC cells to gefitinib and inducing apoptosis. MiR-345 and miR-498 were verified to inhibit proliferation by cell cycle arrest and regulate the MAPK/c-Fos and AKT/Bcl-2 signalling pathways by directly targeting MAPK1 and PIK3R1 respectively. The combination of TMS and gefitinib promoted apoptosis also by miR-345 and miR-498 targeting the MAPK/c-Fos and AKT/Bcl-2 signalling pathways. Our study demonstrated that TMS reduced gefitinib resistance in NSCLCs via suppression of the MAPK/Akt/Bcl-2 pathway by upregulation of miR-345/498. These findings would lay the theoretical basis for the future study of TMS for the treatment of EGFR-TKI resistance in NSCLCs.
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