ArticleJournal of experimental & clinical cancer research : CR2025
AZIN1 level is increased in medulloblastoma and correlates with c-Myc activity and tumor phenotype.
Article in Journal of experimental & clinical cancer research : CR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- The Age-Dependent Resident Myonuclear Multi-Omic Response to an Acute Skeletal Muscle Hypertrophic Stimulus in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Age-Dependent Resident Myonuclear Multi-Omic Response to a Skeletal Muscle Hypertrophic Stimulus.bioRxiv : the preprint server for biology · 2025Article
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10 authors.
Funding
Abstract
backgroundAZIN1 is a cell cycle regulator that is upregulated in a variety of cancers. AZIN1 overexpression can induce a more aggressive tumor phenotype via increased binding and resultant inhibition of antizyme. Antizyme is a protein that normally functions as an anti-tumor regulator that facilitates the deactivation of several growth-promoting proteins including c-Myc. MYC plays a critical role in medulloblastoma pathogenesis. Its amplification serves as a defining characteristic of group 3 medulloblastomas, associated with the most aggressive clinical course, greater frequency of metastases, and shorter survival times.
methodsMedulloblastoma tissues (68 TMA, and 45 fresh tissues, and 31 controls) were stained (fluorescence and immunohistochemical) for AZIN1. Western blotting and ELISA were used to detect the AZIN1 level. Phenotypically aggressive cellular features were measured by increased invasion, colony formation and proliferation. CRISPR-Cas9-mediated AZIN1 knocked-out cells were orthotopically implanted in the cerebellum of nude mice (n = 8/group) with a stereotactic frame. Tumor growth was monitored using the In Vivo Imaging System (IVIS).
resultsHere, we investigated the role of AZIN1 expression in medulloblastoma. We found that overexpression of AZIN1 in medulloblastoma cells induces phenotypically aggressive features. Conducting in vivo studies we found that knocking-out AZIN1 in tumors corresponds with reduced tumor progression and prolonged survival. Clinical specimens are revealing that AZIN1 is highly expressed and directly correlates with MYC amplification status in patients.
conclusionThese data implicate AZIN1 as a putative regulator of medulloblastoma pathogenesis and suggest that it may have clinical application as both a biomarker and novel therapeutic target.
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