ArticleOncotarget2017
NUP37, a positive regulator of YAP/TEAD signaling, promotes the progression of hepatocellular carcinoma.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The trial behind it
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- ASCL1 promotes nuclear shrinkage in transdifferentiation by suppressing NUP37.Stem cell reports · 2026Article
- Transcriptomic insights into developmental arrest in fluorescent labeling transgenic Asian elephant (Frontiers in cell and developmental biology · 2025Article
- NUP37 promotes the proliferation and invasion of glioma cells through DNMT1-mediated methylation.Cell death discovery · 2024Article
- Advances in the understanding of nuclear pore complexes in human diseases.Journal of cancer research and clinical oncology · 2024Review
- The role of the FSGS disease gene product and nuclear pore protein NUP205 in regulating nuclear localization and activity of transcriptional regulators YAP and TAZ.Human molecular genetics · 2023Article
- Nuclear Import and Export of YAP and TAZ.Cancers · 2023Review
- Article
- A Proteomic Approach to Study the Biological Role of Hepatitis C Virus Protein Core+1/ARFP.Viruses · 2022Article
- Identification of Co-Expression Modules and Genes Associated With Tumor Progression in Oral Squamous Cell Carcinoma.Pathology oncology research : POR · 2022Article
- The function of Nucleoporin 37 on mouse oocyte maturation and preimplantation embryo development.Journal of assisted reproduction and genetics · 2022Article
- Nucleoporin 37 promotes the cell proliferation, migration, and invasion of gastric cancer through activating the PI3K/AKT/mTOR signaling pathway.In vitro cellular & developmental biology. Animal · 2021Article
- Significantly high expression of NUP37 leads to poor prognosis of glioma patients by promoting the proliferation of glioma cells.Cancer medicine · 2021Article
- Transcatheter arterial chemoembolization combined with Hippo/YAP inhibition significantly improve the survival of rats with transplanted hepatocellular carcinoma.Lipids in health and disease · 2021Article
- Diamond Nanofilm Normalizes Proliferation and Metabolism in Liver Cancer Cells.Nanotechnology, science and applications · 2021Article
- Evaluation of Oncogene NUP37 as a Potential Novel Biomarker in Breast Cancer.Frontiers in oncology · 2021Article
- The Yin and Yang of Autosomal Recessive Primary Microcephaly Genes: Insights from Neurogenesis and Carcinogenesis.International journal of molecular sciences · 2020Review
- The HIPPO Transducer YAP and Its Targets CTGF and Cyr61 Drive a Paracrine Signalling in Cold Atmospheric Plasma-Mediated Wound Healing.Oxidative medicine and cellular longevity · 2020Article
- Deletion of low-density lipoprotein-related receptor 5 inhibits liver Cancer cell proliferation via destabilizing Nucleoporin 37.Cell communication and signaling : CCS · 2019Article
- Moderate Nucleoporin 133 deficiency leads to glomerular damage in zebrafish.Scientific reports · 2019Article
- Mechanosensing at the Nuclear Envelope by Nuclear Pore Complex Stretch Activation and Its Effect in Physiology and Pathology.Frontiers in physiology · 2019Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of YAP/TEAD signaling is very common in the progression of HCC (Hepatocellular carcinoma). Nuclear pore complex (NPC) regulates the shuttling of proteins between cytoplasm and nucleus. Nuclear accumulation of YAP protein has been observed in the majority of HCC tissues. However, whether NPC could regulate the YAP/TEAD signaling remains unknown. In this study, it was found NUP37, the component of NPC, significantly up-regulated in HCC clinical samples and mouse model. Over-expression of NUP37 promoted the growth, migration and invasion of HCC cells, while knocking down the expression of NUP37 inhibited the growth, migration, invasion and metastasis of HCC cells and improved the survival of the mouse model. NUP37 interacted with YAP and activated YAP/TEAD signaling by enhancing the interaction between YAP and TEAD. Taken together, these data demonstrated the oncogenic roles of NUP37 in the progression of HCC and suggested that NUP37 might be a promising therapeutic target.
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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.