ArticleOncotarget2016
Protein 4.1N acts as a potential tumor suppressor linking PP1 to JNK-c-Jun pathway regulation in NSCLC.
Article in Oncotarget, 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 20 papers.
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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
20 citing papers in PubMed, 28 citations in OpenAlex.
- Noncoding RNAs as regulators of FOSL1 in cancer.Frontiers in immunology · 2025Review
- EphA-Mediated Regulation of Stomatin Expression in Prostate Cancer Cells.Cancer medicine · 2024Article
- IKKα promotes lung adenocarcinoma growth through ERK signaling activation via DARPP-32-mediated inhibition of PP1 activity.NPJ precision oncology · 2023Article
- Tumor Suppressor 4.1N/Frontiers in genetics · 2022Article
- Morphine promotes the malignant biological behavior of non-small cell lung cancer cells through the MOR/Src/mTOR pathway.Cancer cell international · 2021Article
- Loss of 4.1N in epithelial ovarian cancer results in EMT and matrix-detached cell death resistance.Protein & cell · 2021Article
- 4.1N-Mediated Interactions and Functions in Nerve System and Cancer.Frontiers in molecular biosciences · 2021Review
- Antitumor Drug Combretastatin-A4 Phosphate Aggravates the Symptoms of Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice.Frontiers in pharmacology · 2020Article
- Mechanism of microRNA-431-5p-Archives of medical science : AMS · 2019Article
- Expression of Protein 4.1 Family in Breast Cancer: Database Mining for 4.1 Family Members in Malignancies.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- C-myc/miR-150/EPG5 axis mediated dysfunction of autophagy promotes development of non-small cell lung cancer.Theranostics · 2019Article
- Targeting c-met receptor tyrosine kinase by the DNA aptamer SL1 as a potential novel therapeutic option for myeloma.Journal of cellular and molecular medicine · 2018Article
- Protein 4.1N is required for the formation of the lateral membrane domain in human bronchial epithelial cells.Biochimica et biophysica acta. Biomembranes · 2018Article
- miR-145-5p inhibits epithelial-mesenchymal transition via the JNK signaling pathway by targeting MAP3K1 in non-small cell lung cancer cells.Oncology letters · 2017Article
- MiR-150 promotes cellular metastasis in non-small cell lung cancer by targeting FOXO4.Scientific reports · 2016Article
- Follistatin-like protein 1 contributes to dendritic cell and T-lymphocyte activation in nasopharyngeal carcinoma patients by altering nuclear factor κb and Jun N-terminal kinase expression.Cell biochemistry and function · 2016Article
- microRNA-590 suppresses the tumorigenesis and invasiveness of non-small cell lung cancer cells by targeting ADAM9.Molecular and cellular biochemistry · 2016Article
- The Fra-1-miR-134-SDS22 feedback loop amplifies ERK/JNK signaling and reduces chemosensitivity in ovarian cancer cells.Cell death & disease · 2016Article
- 4.1N is involved in a flotillin-1/β-catenin/Wnt pathway and suppresses cell proliferation and migration in non-small cell lung cancer cell lines.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- c-Jun N-terminal kinase activation has a prognostic implication and is negatively associated with FOXO1 activation in gastric cancer.BMC gastroenterology · 2016Article
Corrections and comments
- Erratum issued
Authors and funding
19 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein 4.1N is a member of protein 4.1 family and has been recognized as a potential tumor suppressor in solid tumors. Here, we aimed to investigate the role and mechanisms of 4.1N in non-small cell lung cancer (NSCLC). We confirmed that the expression level of 4.1N was inversely correlated with the metastatic properties of NSCLC cell lines and histological grade of clinical NSCLC tissues. Specific knockdown of 4.1N promoted tumor cell proliferation, migration and adhesion in vitro, and tumor growth and metastasis in mouse xenograft models. Furthermore, we identified PP1 as a novel 4.1N-interacting molecule, and the FERM domain of 4.1N mediated the interaction between 4.1N and PP1. Further, ectopic expression of 4.1N could inactivate JNK-c-Jun signaling pathway through enhancing PP1 activity and interaction between PP1 and p-JNK. Correspondingly, expression of potential downstream metastasis targets (ezrin and MMP9) and cell cycle targets (p53, p21 and p19) of JNK-c-Jun pathway were also regulated by 4.1N. Our data suggest that down-regulation of 4.1N expression is a critical step for NSCLC development and that repression of JNK-c-Jun signaling through PP1 is one of the key anti-tumor mechanisms of 4.1N.
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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.