ArticleNeoplasia (New York, N.Y.)2016
PIAS1-FAK Interaction Promotes the Survival and Progression of Non-Small Cell Lung Cancer.
Article in Neoplasia (New York, N.Y.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 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
21 citing papers in PubMed, 30 citations in OpenAlex.
- Focal adhesion kinase: A promising regulator of colitis-associated healing.World journal of gastroenterology · 2025Review
- Comprehensive multimodal and multiomic profiling reveals epigenetic and transcriptional reprogramming in lung tumors.Communications biology · 2025Article
- TRIM72 inhibits cell migration and epithelial-mesenchymal transition by attenuating FAK/akt signaling in colorectal cancer.Heliyon · 2024Article
- PIAS family gene expression: implications for prognosis, immunomodulation, and chemotherapy response.American journal of translational research · 2024Article
- PIAS family in cancer: from basic mechanisms to clinical applications.Frontiers in oncology · 2024Review
- Focal adhesion kinase: from biological functions to therapeutic strategies.Experimental hematology & oncology · 2023Review
- The emerging roles of SUMOylation in pulmonary diseases.Molecular medicine (Cambridge, Mass.) · 2023Review
- Cancer-Associated Dysregulation of Sumo Regulators: Proteases and Ligases.International journal of molecular sciences · 2022Review
- Identification of genes and pathways leading to poor prognosis of non-small cell lung cancer using integrated bioinformatics analysis.Translational cancer research · 2022Article
- Clinical Roles of Risk Model Based on Differentially Expressed Genes in Mesenchymal Stem Cells in Prognosis and Immunity of Non-small Cell Lung Cancer.Frontiers in genetics · 2022Article
- Review
- Article
- Article
- Inhibition of protein FAK enhances 5-FU chemosensitivity to gastric carcinomaComputational and structural biotechnology journal · 2020Article
- Role of Focal Adhesion Kinase in Small-Cell Lung Cancer and Its Potential as a Therapeutic Target.Cancers · 2019Review
- Increased Expression and Activation of FAK in Small-Cell Lung Cancer Compared to Non-Small-Cell Lung Cancer.Cancers · 2019Article
- The roles of nuclear focal adhesion kinase (FAK) on Cancer: a focused review.Journal of experimental & clinical cancer research : CR · 2019Review
- Identification of the targets of hematoporphyrin derivative in lung adenocarcinoma using integrated network analysis.Biological research · 2019Article
- Therapeutic Potential of Focal Adhesion Kinase Inhibition in Small Cell Lung Cancer.Molecular cancer therapeutics · 2019Article
- miR-138 suppresses the proliferation, metastasis and autophagy of non-small cell lung cancer by targeting Sirt1.Oncology reports · 2017Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
The sequence of genomic alterations acquired by cancer cells during tumor progression and metastasis is poorly understood. Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that integrates cytoskeleton remodeling, mitogenic signaling and cell survival. FAK has previously been reported to undergo nuclear localization during cell migration, cell differentiation and apoptosis. However, the mechanism behind FAK nuclear accumulation and its contribution to tumor progression has remained elusive. We report that amplification of FAK and the SUMO E3 ligase PIAS1 gene loci frequently co-occur in non-small cell lung cancer (NSCLC) cells, and that both gene products are enriched in a subset of primary NSCLCs. We demonstrate that endogenous FAK and PIAS1 proteins interact in the cytoplasm and the cell nucleus of NSCLC cells. Ectopic expression of PIAS1 promotes proteolytic cleavage of the FAK C-terminus, focal adhesion maturation and FAK nuclear localization. Silencing of PIAS1 deregulates focal adhesion turnover, increases susceptibility to apoptosis in vitro and impairs tumor xenograft formation in vivo. Nuclear FAK in turn stimulates gene transcription favoring DNA repair, cell metabolism and cytoskeleton regulation. Consistently, ablation of FAK by CRISPR/Cas9 editing, results in basal DNA damage, susceptibility to ionizing radiation and impaired oxidative phosphorylation. Our findings provide insight into a mechanism regulating FAK cytoplasm-nuclear distribution and demonstrate that FAK activity in the nucleus promotes NSCLC survival and progression by increasing cell-ECM interaction and DNA repair regulation.
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.