ArticleCancer cell international2022
ZMIZ2 promotes the development of triple-receptor negative breast cancer.
Article in Cancer cell international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Interaction between ZMIZ2 and AR promotes prostate cancer proliferation in vitro and in vivo.Cancer biology & therapy · 2026Article
- Artificial Intelligence-Driven Construction of Predictive and Druggable Frameworks to an In Silico Bioengineering Evidence Support for Therapy of Esophageal Squamous Cell Carcinoma Patients: Insights from a Toll-like Receptor Signal with Th17 and T Helper Microenvironment.Bioengineering (Basel, Switzerland) · 2026Article
- Cross-generational transcriptomic effects of alcohol use disorder in third generation offspring.Scientific reports · 2026Article
- Integrating network analysis and machine learning to explore the pharmacological targets and associations of oleanolic acid in lung adenocarcinoma.Frontiers in pharmacology · 2026Article
- ZMIZ2 interacts with PIN1 to promote lung adenocarcinoma EMT and metastasis via activation of the PI3K/AKT pathway.Cell & bioscience · 2025Article
- A silence catalyst: CCL5-mediated intercellular communication in cancer.Archives of toxicology · 2025Review
- ZMIZ2/MCM3 Axis Participates in Triple-Negative Breast Cancer Progression.Oncology research · 2025Article
- Expression of gamma-aminobutyric acid type A receptor subunit π and minichromosome maintenance-3 in breast cancer patients treated with neoadjuvant chemotherapy: a target molecule or a proliferation marker?Revista da Associacao Medica Brasileira (1992) · 2025Article
- Identification of zinc finger MIZ-type containing 2 as an oncoprotein enhancing NAD-dependent protein deacetylase sirtuin-1 deacetylase activity to regulate Wnt and Hippo pathways in non-small-cell lung cancer.Cellular & molecular biology letters · 2024Article
- ZMIZ2 facilitates hepatocellular carcinoma progression via LEF1 mediated activation of Wnt/β-catenin pathway.Experimental hematology & oncology · 2024Article
- Gene expression profile analysis to discover molecular signatures for early diagnosis and therapies of triple-negative breast cancer.Frontiers in molecular biosciences · 2022Article
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundTriple-receptor negative breast cancer (TNBC) is an aggressive breast tumor subtype that generally has a poor prognosis. This study aimed to investigate the role and regulatory mechanisms of Zinc finger MIZ-type containing 2 (ZMIZ2) in relation to TNBC.
methodsBased on data from The Cancer Genome Atlas (TCGA), the expression of ZMIZ2 in different subtypes and its correlation with androgen receptor (AR) were analyzed, and a regulatory mechanism network was constructed. The expression and prognostic value of ZMIZ2 in clinical TNBC tissue samples were also investigated. Furthermore, in vitro studies were conducted to investigate the effects of ZMIZ2 knockdown on the malignant behaviors of TNBC cells and target gene expression.
resultsBased on TCGA data, ZMIZ2 was found to be significantly upregulated in TNBC tissues and its expression was negatively correlated with AR expression. Key relationships, such as the ZMIZ2-CCL5, ZMIZ2/AR-MCM3, ZMIZ2/AR-E2F4, and the ZMIZ2/AR-DHX38 were identified, which were enriched in NOD-like receptor signaling pathway/toll-like receptor signaling pathway, DNA replication, cell cycle, and spliceosome, respectively. Moreover, ZMIZ2 was upregulated in clinical breast cancer tissues and its high expression was correlated with the poor prognosis of TNBC patients. Furthermore, ZMIZ2 expression was increased in breast cancer cells, and a knockdown of ZMIZ2 inhibited MDA-MB-231 cell proliferation, migration, and invasion, induced cell cycle arrest in the G1 phase, and promoted cell apoptosis. Furthermore, ZMIZ2 knockdown inhibited the mRNA and protein expression of CCL5, MCM3, E2F4, and DHX38.
conclusionOur findings reveal that ZMIZ2 is upregulated in TNBC tissues and is associated with its poor prognosis. ZMIZ2 may promote TNBC progression by promoting the expression of its target genes and affecting the corresponding pathways. Consequently, ZMIZ2 may serve as a promising target for future TNBC treatments.
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