ArticleCancer research communications2022
Smoking-associated Downregulation of FILIP1L Enhances Lung Adenocarcinoma Progression Through Mucin Production, Inflammation, and Fibrosis.
Article in Cancer research communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Dynamic microbiome-host interactions and their associations with systemic metabolism and radiological characteristics during early lung adenocarcinoma.NPJ precision oncology · 2026Article
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- Improvement of machine learning models for predicting high-grade subtypes of lung adenocarcinoma based on delta radiomics: A multicenter cohort study.European journal of radiology open · 2025Article
- PFDN1 silencing disrupts critical cancer pathways in triple-negative breast cancer: investigating migration, cell cycle, and apoptosis as a new target therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Orthotopically Implanted Murine Lung Adenocarcinoma Cell Lines for Preclinical Investigations.Cancers · 2025Review
- The multifaceted roles of mucins family in lung cancer: from prognostic biomarkers to promising targets.Frontiers in immunology · 2025Review
- A Comprehensive Analysis of the ceRNA Network and Hub Genes in Avian Leukosis Virus Subgroup J and Infectious Bursal Disease Virus Superinfection.Animals : an open access journal from MDPI · 2024Article
- Comprehensive evaluation of smoking exposures and their interactions on DNA methylation.EBioMedicine · 2024Article
- Decoding tumor-fibrosis interplay: mechanisms, impact on progression, and innovative therapeutic strategies.Frontiers in pharmacology · 2024Review
- Decoding the Gene Regulatory Network of Muscle Stem Cells in Mouse Duchenne Muscular Dystrophy: Revelations from Single-Nuclei RNA Sequencing Analysis.International journal of molecular sciences · 2023Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Lung adenocarcinoma (LUAD) is the major subtype in lung cancer, and cigarette smoking is essentially linked to its pathogenesis. We show that downregulation of Filamin A interacting protein 1-like (FILIP1L) is a driver of LUAD progression. Cigarette smoking causes its downregulation by promoter methylation in LUAD. Loss of FILIP1L increases xenograft growth, and, in lung-specific knockout mice, induces lung adenoma formation and mucin secretion. In syngeneic allograft tumors, reduction of FILIP1L and subsequent increase in its binding partner, prefoldin 1 (PFDN1) increases mucin secretion, proliferation, inflammation, and fibrosis. Importantly, from the RNA-sequencing analysis of these tumors, reduction of FILIP1L is associated with upregulated Wnt/β-catenin signaling, which has been implicated in proliferation of cancer cells as well as inflammation and fibrosis within the tumor microenvironment. Overall, these findings suggest that down-regulation of FILIP1L is clinically relevant in LUAD, and warrant further efforts to evaluate pharmacologic regimens that either directly or indirectly restore FILIP1L-mediated gene regulation for the treatment of these neoplasms. Significance: This study identifies FILIP1L as a tumor suppressor in LUADs and demonstrates that downregulation of FILIP1L is a clinically relevant event in the pathogenesis and clinical course of these neoplasms.
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