ArticleCell death & disease2016
ANP32B deficiency impairs proliferation and suppresses tumor progression by regulating AKT phosphorylation.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- The disulfonic acid ANDS disrupts ANP32B-p53 interaction to suppress chronic myeloid leukemia.Nature communications · 2026Article
- Integrated single-cell and spatial mapping coupled with machine learning unveils core stemness landscapes and regulatory drivers in triple-negative breast cancer.Discover oncology · 2026Article
- Integrating multimodal cancer data using deep latent variable path modelling.Nature machine intelligence · 2025Article
- ANP32B promotes colorectal cancer cell progression and reduces cell sensitivity to PRAP1 inhibitor through up-regulating HPF1.Heliyon · 2024Article
- ANP32B suppresses B-cell acute lymphoblastic leukemia through activation of PU.1 in mice.Cancer science · 2023Article
- ArtinM Cytotoxicity in B Cells Derived from Non-Hodgkin's Lymphoma Depends on Syk and Src Family Kinases.International journal of molecular sciences · 2023Article
- BRD4 PROTAC degrader MZ1 exerts anticancer effects in acute myeloid leukemia by targeting c-Myc and ANP32B genes.Cancer biology & therapy · 2022Article
- ANP32 Family as Diagnostic, Prognostic, and Therapeutic Biomarker Related to Immune Infiltrates in Hepatocellular Carcinoma.Disease markers · 2022Article
- ANP32B-mediated repression of p53 contributes to maintenance of normal and CML stem cells.Blood · 2021Article
- NANOS2 suppresses the cell cycle by repressing mTORC1 activators in embryonic male germ cells.iScience · 2021Article
- Metalloproteomics analysis in human mammary cell lines treated with inorganic mercury.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2020Article
- ANP32B Deficiency Protects Mice From Lethal Influenza A Virus Challenge by Dampening the Host Immune Response.Frontiers in immunology · 2020Article
- Identifying Methylation Pattern and Genes Associated with Breast Cancer Subtypes.International journal of molecular sciences · 2019Article
- Stoichiogenomics reveal oxygen usage bias, key proteins and pathways associated with stomach cancer.Scientific reports · 2019Article
- The acidic protein rich in leucines Anp32b is an immunomodulator of inflammation in mice.Scientific reports · 2019Article
- A component overlapping attribute clustering (COAC) algorithm for single-cell RNA sequencing data analysis and potential pathobiological implications.PLoS computational biology · 2019Article
- Che-1 is targeted by c-Myc to sustain proliferation in pre-B-cell acute lymphoblastic leukemia.EMBO reports · 2018Article
- Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The acidic leucine-rich nuclear phosphoprotein 32B (ANP32B) is reported to impact normal development, with Anp32b-knockout mice exhibiting smaller size and premature aging. However, its cellular and molecular mechanisms, especially its potential roles in tumorigenesis, remain largely unclear. Here, we utilize 'knockout' models, RNAi silencing and clinical cohorts to more closely investigate the role of this enigmatic factor in cell proliferation and cancer phenotypes. We report that, compared with Anp32b wild-type (Anp32b(+/+)) littermates, a broad panel of tissues in Anp32b-deficient (Anp32b(-/-)) mice are demonstrated hypoplasia. Anp32b(-/-) mouse embryo fibroblast cell has a slower proliferation, even after oncogenic immortalization. ANP32B knockdown also significantly inhibits in vitro and in vivo growth of cancer cells by inducing G1 arrest. In line with this, ANP32B protein has higher expression in malignant tissues than adjacent normal tissues from a cohort of breast cancer patients, and its expression level positively correlates with their histopathological grades. Moreover, ANP32B deficiency downregulates AKT phosphorylation, which involves its regulating effect on cell growth. Collectively, our findings suggest that ANP32B is an oncogene and a potential therapeutic target for breast cancer treatment.
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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.