ArticleGenes & genomics2023
ANXA3, associated with YAP1 regulation, participates in the proliferation and chemoresistance of cervical cancer cells.
Article in Genes & genomics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 2 citations in OpenAlex.
- Transcriptional activation of GSTP1 by ANXA3 is associated with cisplatin sensitivity in colorectal cancer cells.Oncology letters · 2026Article
- FOXD1-activated ANXA3 facilitates cisplatin resistance of lung cancer cells via promoting ANXA4 expression.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Two cases of mixed large cell neuroendocrine carcinoma and adenocarcinoma of the cervix: case report and review of the literature.Diagnostic pathology · 2024Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundCervical cancer, as one of the most common cancers in women, remains a major health threat worldwide. Annexin A3 (ANXA3), a component of the annexin family, is upregulated in numerous cancers, with no explicit role in cervical cancer.
objectiveThis study aims to investigate the function of ANXA3 in cervical cancer.
methodsDifferential expression genes between the cervical cancer tissues of patients and the controls were analyzed in The Cancer Genome Atlas (TCGA) and Gene Expression Profiling Interactive Analysis (GEPIA) database. Using transfection approaches to either upregulate or downregulate ANXA3, its role in cell proliferation and chemosensitivity of human cervical cancer cell lines (HeLa and C33A) was evaluated. Furthermore, the binding activity between YAP1 and ANXA3 was also explored.
resultsGenomics analysis indicated that differential genes were mostly associated with cell cycle progression and DNA replication. ANXA3 was highly expressed in the cervical cancer tissues and closely linked to malignancy degree. Knockdown of ANXA3 in cervical cancer cells inhibited cell cycle progression. A similar result was observed in the reduction of cyclin D, CDK4, cyclin E, and CDK2 in cervical cancer cells with ANXA3 silencing. Cervical cancer cells obtained high sensitivity to cisplatin (DDP) when ANXA3 was downregulated. Conversely, these capabilities were the opposite in cervical cancer cells overexpressing ANXA3. Furthermore, the expression levels of ANXA3 and YAP1 were positively correlated. YAP1 upregulation was positively connected with malignant behaviors, which were reversed by ANXA3 downregulation.
conclusionIn light of our findings, targeting ANXA3 expressed in cervical cancer might contribute to more potential therapeutic strategies.
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