ArticleCancer research2014
MUC1 in macrophage: contributions to cigarette smoke-induced lung cancer.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 26 citations in OpenAlex.
- Integrated Network and Transcriptomic Analyses Identify a Candidate Ethanol-ADAM17 Molecular Axis Associated with Glioblastoma Progression.International journal of molecular sciences · 2026Article
- Multiple roles and mechanisms of MUC6 in cancer (Review).International journal of molecular medicine · 2025Review
- ARID1A silencing-mediated upregulation of microRNA-652 accelerates cigarette smoke-induced human bronchial epithelial cell transformation by targeting ZFAND5.BMC pulmonary medicine · 2025Article
- Therapeutic Vaccination in Lung Cancer: Past Attempts, Current Approaches and Future Promises.Journal of respiratory biology and translational medicine · 2025Article
- The Role of MRE11 in the IL-6/STAT3 Pathway of Lung Cancer Cells.Current issues in molecular biology · 2022Article
- Polymorphism ofFrontiers in oncology · 2021Article
- Comprehensive analysis of gene expression and DNA methylation data identifies potential biomarkers and functional epigenetic modules for lung adenocarcinoma.Genetics and molecular biology · 2020Article
- Vasorin/ATIA Promotes Cigarette Smoke-Induced Transformation of Human Bronchial Epithelial Cells by Suppressing Autophagy-Mediated Apoptosis.Translational oncology · 2020Article
- Picket-fences in the plasma membrane: functions in immune cells and phagocytosis.Seminars in immunopathology · 2018Review
- Cigarette Smoking-Mediated Macrophage Reprogramming: Mechanistic Insights and Therapeutic Implications.Journal of nature and science · 2018Article
- MUC1: The First Respiratory Mucin with an Anti-Inflammatory Function.Journal of clinical medicine · 2017Review
- Danshen improves survival of patients with advanced lung cancer and targeting the relationship between macrophages and lung cancer cells.Oncotarget · 2017Article
- Muc1 knockout potentiates murine lung carcinogenesis involving an epiregulin-mediated EGFR activation feedback loop.Carcinogenesis · 2017Article
- Mucin-1 correlates with survival, smoking status, and growth patterns in lung adenocarcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Modulation of macrophage polarization and lung cancer cell stemness by MUC1 and development of a related small-molecule inhibitor pterostilbene.Oncotarget · 2016Article
- FleA Expression in Aspergillus fumigatus Is Recognized by Fucosylated Structures on Mucins and Macrophages to Prevent Lung Infection.PLoS pathogens · 2016Article
- Membrane-Tethered MUC1 Mucin Counter-Regulates the Phagocytic Activity of Macrophages.American journal of respiratory cell and molecular biology · 2016Article
- IKBKE Upregulation is Positively Associated with Squamous Cell Carcinoma of the Lung In Vivo and Malignant Transformation of Human Bronchial Epithelial Cells In Vitro.Medical science monitor : international medical journal of experimental and clinical research · 2015Article
- A signaling pathway consisting of miR-551b, catalase and MUC1 contributes to acquired apoptosis resistance and chemoresistance.Carcinogenesis · 2014Article
- Measurement of TACE Activity in Extracts from Cultured Cells.Bio-protocol · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Expression of the pro-oncogenic mucin MUC1 is elevated by inflammation in airway epithelial cells, but the contributions of MUC1 to the development of lung cancer are uncertain. In this study, we developed our finding that cigarette smoke increases Muc1 expression in mouse lung macrophages, where we hypothesized MUC1 may contribute to cigarette smoke-induced transformation of bronchial epithelial cells. In human macrophages, cigarette smoke extract (CSE) strongly induced MUC1 expression through a mechanism involving the nuclear receptor PPAR-γ. CSE-induced extracellular signal-regulated kinase (ERK) activation was also required for MUC1 expression, but it had little effect on MUC1 transcription. RNA interference-mediated attenuation of MUC1 suppressed CSE-induced secretion of TNF-α from macrophages, by suppressing the activity of the TNF-α-converting enzyme (TACE), arguing that MUC1 is required for CSE-induced and TACE-mediated TNF-α secretion. Similarly, MUC1 blockade after CSE induction through suppression of PPAR-γ or ERK inhibited TACE activity and TNF-α secretion. Conditioned media from CSE-treated macrophages induced MUC1 expression and potentiated CSE-induced transformation of human bronchial epithelial cells in a TNF-α-dependent manner. Together, our results identify a signaling pathway involving PPAR-γ, ERK, and MUC1 for TNF-α secretion induced by CSE from macrophages. Furthermore, our results show how MUC1 contributes to smoking-induced lung cancers that are driven by inflammatory signals from macrophages.
Indexed as
Identifiers
What OpenQuestion holds
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.