ArticleCancer biomarkers : section A of Disease markers2022
Curcumin increases crizotinib sensitivity through the inactivation of autophagy via epigenetic modulation of the miR-142-5p/Ulk1 axis in non-small cell lung cancer.
Article in Cancer biomarkers : section A of Disease markers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.
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Who cites it
16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 21 citations in OpenAlex.
- Combination Chemotherapy with Selected Polyphenols in Preclinical and Clinical Studies-An Update Overview.Molecules (Basel, Switzerland) · 2023Pooled it
- Pooled it
- Curcumin and Cancer Stem Cells: Epigenetic Mechanisms Underlying Therapeutic Resistance and Tumor Relapse.International journal of molecular sciences · 2026Review
- ROS and Antioxidants: Prospective Therapeutic Options in Cancer.Journal of cellular and molecular medicine · 2026Article
- Phytochemical-Based Strategies for Lung Cancer: Clinical Insights Into Pleiotropic Molecular Signaling and Therapeutic Roles.Phytotherapy research : PTR · 2026Review
- Non-small cell lung cancer after EGFR-TKI resistance: from drug resistance mechanisms to precision interventions.Frontiers in pharmacology · 2026Review
- Targeting the Epigenetic Landscape for Lung Cancer Treatment.Journal of cellular and molecular medicine · 2025Article
- Article
- The potential of targeting autophagy-related non-coding RNAs in the treatment of lung cancer.Frontiers in pharmacology · 2025Review
- Drugging the tumor microenvironment epigenome for therapeutic interventions in NSCLC.Journal of Cancer · 2025Article
- Harnessing the Power of Polyphenols: A New Frontier in Disease Prevention and Therapy.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Regulatory miRNAs in cancer cell recovery from therapy exposure and its implications as a novel therapeutic strategy for preventing disease recurrence.The Enzymes · 2023Article
- Circulating miRNA Expression Profiles and Machine Learning Models in Association with Response to Irinotecan-Based Treatment in Metastatic Colorectal Cancer.International journal of molecular sciences · 2022Article
- Curcumin and Its Analogs in Non-Small Cell Lung Cancer Treatment: Challenges and Expectations.Biomolecules · 2022Review
- Focusing on the Role of Natural Products in Overcoming Cancer Drug Resistance: An Autophagy-Based Perspective.Biomolecules · 2022Review
- Using ncRNAs as Tools in Cancer Diagnosis and Treatment-The Way towards Personalized Medicine to Improve Patients' Health.International journal of molecular sciences · 2022Review
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Authors and funding
13 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drug resistance is a critical factor responsible for the recurrence of non-small cell lung cancer (NSCLC). Previous studies suggest that curcumin acts as a chemosensitizer and radiosensitizer in human malignancies, but the underlying mechanism remains elusive. In the present study, we explored how curcumin regulates the expression of miR-142-5p and sensitizes NSCLC cells to crizotinib. We found that miR-142-5p is significantly downregulated in NSCLC tissue samples and cell lines. Curcumin could increase crizotinib cytotoxicity by epigenetically restoring the expression of miR-142-5p. Furthermore, curcumin treatment suppressed the expression of DNA methylation-related enzymes, including DNMT1, DNMT3A, and DNMT3B, in NSCLC cells. In addition, the upregulation of miR-142-5p expression increased crizotinib cytotoxicity and induced apoptosis in tumor cells in a similar manner to that of curcumin. Strikingly, miR-142-5p overexpression suppressed crizotinib-induced autophagy in A549 and H460 cells. Mechanistically, miR-142-5p inhibited autophagy in lung cancer cells by targeting Ulk1. Overexpression of Ulk1 abrogated the miR-142-5p-induced elevation of crizotinib cytotoxicity in A549 and H460 cells. Collectively, our findings demonstrate that curcumin sensitizes NSCLC cells to crizotinib by inactivating autophagy through the regulation of miR-142-5p and its target Ulk1.
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