ArticleCancer research2012
Mithramycin represses basal and cigarette smoke-induced expression of ABCG2 and inhibits stem cell signaling in lung and esophageal cancer cells.
Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 98 citations in OpenAlex.
- Esophageal cancer: from pathogenesis to precision therapies.Signal transduction and targeted therapy · 2026Review
- Repression of ZNFX1 by LncRNA ZFAS1 mediates tobacco-induced pulmonary carcinogenesis.Cellular & molecular biology letters · 2025Article
- Endoscopic ultrasound-based radiomics for predicting pathologic upgrade in esophageal low-grade intraepithelial neoplasia.Surgical endoscopy · 2025Article
- PCMR: a comprehensive precancerous molecular resource.Scientific data · 2025Article
- Mithramycin targets head and neck cancer stem cells by inhibiting Sp1 and UFMylation.Cancer cell international · 2024Article
- Cholesterol neutralized vemurafenib treatment by promoting melanoma stem-like cells via its metabolite 27-hydroxycholesterol.Cellular and molecular life sciences : CMLS · 2024Article
- Differential Expression of SRY-Related HMG-Box Transcription Factor 2, Oligodendrocyte Lineage Transcription Factor 2, and Zinc Finger E-Box Binding Homeobox 1 in Serum-Derived Extracellular Vesicles: Implications for Mithramycin Sensitivity and Targeted Therapy in High-Grade Glioma.ACS pharmacology & translational science · 2024Article
- Illuminating Shared Genetic Associations Between Oesophageal Carcinoma and Pulmonary Carcinoma Risk.Journal of Cancer · 2024Article
- ABCG2 transporter reduces protein aggregation in cigarette smoke condensate-exposed A549 lung cancer cells.PloS one · 2024Article
- Progress of Cancer Stem Cells in Retinoblastoma.Current stem cell research & therapy · 2024Review
- Cigarette Smoke Enhances the Malignant Phenotype of Esophageal Adenocarcinoma Cells by Disrupting a Repressive Regulatory Interaction Between miR-145 and LOXL2.Laboratory investigation; a journal of technical methods and pathology · 2023Article
- Destroying the Shield of Cancer Stem Cells: Natural Compounds as Promising Players in Cancer Therapy.Journal of clinical medicine · 2022Review
- Lung Cancer Stem Cell Markers as Therapeutic Targets: An Update on Signaling Pathways and Therapies.Frontiers in oncology · 2022Review
- Hookah Smoke Mediates Cancer-Associated Epigenomic and Transcriptomic Signatures in Human Respiratory Epithelial Cells.JTO clinical and research reports · 2021Article
- Apatinib suppresses lung cancer stem-like cells by complex interplay between β-catenin signaling and mitochondrial ROS accumulation.Cell death discovery · 2021Article
- Targeting cancer stem cells for reversing therapy resistance: mechanism, signaling, and prospective agents.Signal transduction and targeted therapy · 2021Review
- Review
- MARCKS cooperates with NKAP to activate NF-kB signaling in smoke-related lung cancer.Theranostics · 2021Article
- Review
- Etiology, cancer stem cells and potential diagnostic biomarkers for esophageal cancer.Cancer letters · 2019Review
Corrections and comments
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Authors and funding
20 authors at 4 institutions in 1 country.
Funding
Abstract
Cigarette smoking at diagnosis or during therapy correlates with poor outcome in patients with lung and esophageal cancers, yet the underlying mechanisms remain unknown. In this study, we observed that exposure of esophageal cancer cells to cigarette smoke condensate (CSC) led to upregulation of the xenobiotic pump ABCG2, which is expressed in cancer stem cells and confers treatment resistance in lung and esophageal carcinomas. Furthermore, CSC increased the side population of lung cancer cells containing cancer stem cells. Upregulation of ABCG2 coincided with increased occupancy of aryl hydrocarbon receptor, Sp1, and Nrf2 within the ABCG2 promoter, and deletion of xenobiotic response elements and/or Sp1 sites markedly attenuated ABCG2 induction. Under conditions potentially achievable in clinical settings, mithramycin diminished basal as well as CSC-mediated increases in AhR, Sp1, and Nrf2 levels within the ABCG2 promoter, markedly downregulated ABCG2, and inhibited proliferation and tumorigenicity of lung and esophageal cancer cells. Microarray analyses revealed that mithramycin targeted multiple stem cell-related pathways in vitro and in vivo. Collectively, our findings provide a potential mechanistic link between smoking status and outcome of patients with lung and esophageal cancers, and support clinical use of mithramycin for repressing ABCG2 and inhibiting stem cell signaling in thoracic malignancies.
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Registered trials
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