ArticleOncotarget2016
NFIB overexpression cooperates with Rb/p53 deletion to promote small cell lung cancer.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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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
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Who cites it
50 citing papers in PubMed, 79 citations in OpenAlex.
- Nanomaterial Strategies for Pulmonary Delivery of Immunotherapeutics in Lung Cancer Treatment.Advanced healthcare materials · 2026Review
- NFIB Regulates Chemoresistance in Small Cell Lung Cancer by Suppressing Notch Signaling Activity.Cancer reports (Hoboken, N.J.) · 2026Article
- EZH2-TTP-mTORC1 Axis Drives Phenotypic Plasticity and Therapeutic Vulnerability in Lethal Prostate Cancer.bioRxiv : the preprint server for biology · 2025Article
- Novel Insights into Emx2 and Dmrta2 Cooperation during Cortex Development and Evidence for Dmrta2 Function in the Choroid Plexus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Challenges of small cell lung cancer heterogeneity and phenotypic plasticity.Nature reviews. Cancer · 2025Review
- The analysis of molecular classification of pulmonary neuroendocrine tumors and relationship between YAP1 and efficacy.Investigational new drugs · 2025Article
- Tumor Heterogeneity and Plasticity in Small Cell Lung Cancer.Lung Cancer (Auckland, N.Z.) · 2025Review
- Roles of the NFI/CTF gene family in transcription and development: update 2025.Academia biology · 2025Article
- Activating Invasion and Metastasis in Small Cell Lung Cancer: Role of the Tumour Immune Microenvironment and Mechanisms of Vasculogenesis, Epithelial-Mesenchymal Transition, Cell Migration, and Organ Tropism.Cancer reports (Hoboken, N.J.) · 2024Review
- Small Cell Lung Cancer Neuronal Features and Their Implications for Tumor Progression, Metastasis, and Therapy.Molecular cancer research : MCR · 2024Review
- Review
- Small Cell Lung Cancer Plasticity Enables NFIB-Independent Metastasis.Cancer research · 2024Article
- Crosstalk between small-cell lung cancer cells and astrocytes mimics brain development to promote brain metastasis.Nature cell biology · 2023Article
- Integrative Analysis of a Large Real-World Cohort of Small Cell Lung Cancer Identifies Distinct Genetic Subtypes and Insights into Histologic Transformation.Cancer discovery · 2023Article
- MicroRNAs associated with postoperative outcomes in patients with limited stage neuroendocrine carcinoma of the esophagus.Oncology letters · 2023Article
- Understanding SCLC heterogeneity and plasticity in cancer metastasis and chemotherapy resistance.Acta biochimica et biophysica Sinica · 2023Review
- The NFIB/CARM1 partnership is a driver in preclinical models of small cell lung cancer.Nature communications · 2023Article
- Identification of TAZ as the essential molecular switch in orchestrating SCLC phenotypic transition and metastasis.National science review · 2022Article
- Killing SCLC: insights into how to target a shapeshifting tumor.Genes & development · 2022Review
- Transcription factor NFIC functions as a tumor suppressor in lung squamous cell carcinoma progression by modulating lncRNA CASC2.Cell cycle (Georgetown, Tex.) · 2022Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Small cell lung cancer (SCLC) is a highly aggressive neuroendocrine tumor type that is typically metastatic upon diagnosis. We have a poor understanding of the factors that control SCLC progression and metastasis. TheNFIB transcription factor is frequently amplified in mouse models of SCLC, but clear evidence that NFIB promotes SCLC in vivo is lacking. We report that in mouse models, Nfib amplifications are far more frequent in liver metastases over primary SCLC, suggesting roles in tumor progression/metastasis. Overexpression of Nfib in a sensitized mouse model led to acceleration of SCLC, indicating that Nfib functions as a bona fide oncogene. Suppression of Nfib expression in cell lines derived from the doxycycline-inducible Rb/p53/TET-Nfib model led to increased apoptosis and suppression of proliferation. Transcriptional analysis revealed that Nfib regulates the expression of genes related to axon guidance, focal adhesion and extracellular matrix-receptor interactions. These data indicate that Nfib is a potent oncogene in SCLC, and the enrichment of Nfib amplifications in liver metastases over primary SCLC points to Nfib as a candidate driver of SCLC metastasis.
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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.