ArticleInternational journal of biological sciences2020
Bisdemethoxycurcumin Enhances the Sensitivity of Non-small Cell Lung Cancer Cells to Icotinib via Dual Induction of Autophagy and Apoptosis.
Article in International journal of biological sciences, 2020. 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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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Progress of ERK Pathway-Modulated Natural Products for Anti-Non-Small-Cell Lung Cancer Activity.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Bisdemethoxycurcumin chemoprevents 7,12-dimethylbenz(a)anthracene-induced mammary toxicity via modulation of oxidative processes.Scientific reports · 2025Article
- Curcuminoids as Cell Signaling Pathway Modulators: A Potential Strategy for Cancer Prevention.Current medicinal chemistry · 2024Review
- Bisdemethoxycurcumin suppresses the progression of atherosclerosis and VSMC-derived foam cell formation by promoting lipophagy.Naunyn-Schmiedeberg's archives of pharmacology · 2023Article
- Bisdemethoxycurcumin alleviates LPS-induced acute lung injury via activating AMPKα pathway.BMC pharmacology & toxicology · 2023Article
- Processing and Physicochemical Properties of Magnetite Nanoparticles Coated withMaterials (Basel, Switzerland) · 2023Article
- Heat treatment-induced autophagy promotes breast cancer cell invasion and metastasis via TGF-PeerJ · 2023Article
- Circulating TP73-AS1 and CRNDE serve as diagnostic and prognostic biomarkers for non-small cell lung cancer.Cancer medicine · 2023Article
- Curcumin and Its Analogs in Non-Small Cell Lung Cancer Treatment: Challenges and Expectations.Biomolecules · 2022Review
- Validation of a Quantification Method for Curcumin Derivatives and Their Hepatoprotective Effects on Nonalcoholic Fatty Liver Disease.Current issues in molecular biology · 2022Article
- Targeted Pyroptosis Is a Potential Therapeutic Strategy for Cancer.Journal of oncology · 2022Review
- Identification of Molecular Targets and Underlying Mechanisms of Xiaoji Recipe against Pancreatic Cancer Based on Network Pharmacology.Computational and mathematical methods in medicine · 2022Article
- Identification of Key Drug Targets and Molecular Mechanisms of Curcumae Rhizoma Acting on HBV-Related HCC: Weighted Correlation Network and Network Pharmacological Analyses.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Synergistic inhibitory effect of berberine and icotinib on non-small cell lung cancer cells via inducing autophagic cell death and apoptosis.Apoptosis : an international journal on programmed cell death · 2021Article
- LncRNA APCDD1L-AS1 induces icotinib resistance by inhibition of EGFR autophagic degradation via the miR-1322/miR-1972/miR-324-3p-SIRT5 axis in lung adenocarcinoma.Biomarker research · 2021Article
- Identification and Validation of Afatinib Potential Drug Resistance GeneFrontiers in oncology · 2021Article
- Resveratrol modulates the apoptosis and autophagic death of human lung adenocarcinoma A549 cells via a p53‑dependent pathway: Integrated bioinformatics analysis and experimental validation.International journal of oncology · 2020Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) wild-type is intrinsic resistance to EGFR-tyrosine kinase inhibitors (TKIs). In this study, we assessed whether the combination of bisdemethoxycurcumin (BDMC) and icotinib could surmount primary EGFR-TKI resistance in NSCLC cells and investigated its molecular mechanism. Results showed that the combination of BDMC and icotinib produced potently synergistic growth inhibitory effect on primary EGFR-TKI-resistant NSCLC cell lines H460 (EGFR wild-type and K-ras mutation) and H1781 (EGFR wild-type and Her2 mutation). Compared with BDMC or icotinib alone, the two drug combination induced more significant apoptosis and autophagy via suppressing EGFR activity and interaction of Sp1 and HDCA1/HDCA2, which was accompanied by accumulation of reactive oxygen species (ROS), induction of DNA damage, and inhibition of cell migration and invasion. ROS inhibitor (NAC) and autophagy inhibitors (CQ or 3-MA) partially reversed BDMC plus icotinib-induced growth inhibitory effect on the NSCLC cells. Meanwhile, co-treatment with NAC attenuated the two drug combination-induced autophagy, apoptosis, DNA damage and decrease of cell migration and invasion ability. Also, 3-MA or CQ can abate the combination treatment-induced apoptosis and DNA damage, suggesting that there is crosstalk between different signaling pathways in the effect produced by the combination treatment. Our data indicate that BMDC has the potential to improve the treatment of primary EGFR-TKI resistant NISCLC that cannot be controlled with single-target agent, such as icotinib.
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