ArticleOncogene2017
Mutant p53 upregulates alpha-1 antitrypsin expression and promotes invasion in lung cancer.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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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.
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Who cites it
35 citing papers in PubMed, 41 citations in OpenAlex.
- New cell lines expanding the diversity of Ewing sarcoma models.International journal of cancer · 2026Article
- Common oncogenic mutations in colorectal cancer: drivers of carcinogenesis and potential therapeutic targets.Frontiers in pharmacology · 2026Review
- Regional profiling reveals a distinct glioblastoma infiltrative margin proteome.Scientific reports · 2025Article
- Alpha-1 antitrypsin promotes re-epithelialization by regulating inflammation and migration.Frontiers in immunology · 2025Article
- Serum α1-AT Levels andDiseases (Basel, Switzerland) · 2024Article
- DNA Damage and Inflammatory Response of p53 Null H358 Non-Small Cell Lung Cancer Cells to X-Ray Exposure Under Chronic Hypoxia.International journal of molecular sciences · 2024Article
- DNA-delivered monoclonal antibodies targeting the p53 R175H mutant epitope inhibit tumor development in mice.Genes & diseases · 2024Article
- A prime editor mouse to model a broad spectrum of somatic mutations in vivo.Nature biotechnology · 2024Article
- Alpha-1 antitrypsin expression is upregulated in multidrug-resistant cancer cells.Histochemistry and cell biology · 2023Article
- Loss of RPA1 Impairs Peripheral T Cell Homeostasis and Exacerbates Inflammatory Damage through Triggering T Cell Necroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- diaPASEF Proteomics and Feature Selection for the Description of Sputum Proteome Profiles in a Cohort of Different Subtypes of Lung Cancer Patients and Controls.International journal of molecular sciences · 2022Article
- Alpha-1 antitrypsin deficiency and risk of lung cancer in never-smokers: a multicentre case-control study.BMC cancer · 2022Article
- Review
- Discovery of bladder cancer biomarkers in paired pre- and postoperative urine samples.Translational andrology and urology · 2021Article
- Auranofin reveals therapeutic anticancer potential by triggering distinct molecular cell death mechanisms and innate immunity in mutant p53 non-small cell lung cancer.Redox biology · 2021Article
- Review
- High DSCC1 Level Predicts Poor Prognosis of Lung Adenocarcinoma.International journal of general medicine · 2021Article
- Mutational drivers of cancer cell migration and invasion.British journal of cancer · 2021Review
- Molecular crosstalk between cancer and neurodegenerative diseases.Cellular and molecular life sciences : CMLS · 2020Review
- Mechanisms behind Retinal Ganglion Cell Loss in Diabetes and Therapeutic Approach.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Missense mutations in the TP53 tumor-suppressor gene inactivate its antitumorigenic properties and endow the incipient cells with newly acquired oncogenic properties that drive invasion and metastasis. Although the oncogenic effect of mutant p53 transcriptome has been widely acknowledged, the global influence of mutant p53 on cancer cell proteome remains to be fully elucidated. Here, we show that mutant p53 drives the release of invasive extracellular factors (the 'secretome') that facilitates the invasion of lung cancer cell lines. Proteomic characterization of the secretome from mutant p53-inducible H1299 human non-small cell lung cancer cell line discovered that the mutant p53 drives its oncogenic pathways through modulating the gene expression of numerous targets that are subsequently secreted from the cells. Of these genes, alpha-1 antitrypsin (A1AT) was identified as a critical effector of mutant p53 that drives invasion in vitro and in vivo, together with induction of epithelial-mesenchymal transition markers expression. Mutant p53 upregulated A1AT transcriptionally through the involvement with its family member p63. Conditioned medium containing secreted A1AT enhanced cell invasion, while an A1AT-blocking antibody attenuated the mutant p53-driven migration and invasion. Importantly, high A1AT expression correlated with increased tumor stage, elevated p53 staining and shorter overall survival in lung adenocarcinoma patients. Collectively, these findings suggest that A1AT is an indispensable target of mutant p53 with prognostic and therapeutic potential in mutant p53-expressing tumors.
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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.