ArticleOncology reports2019
PTEN downregulates WD repeat‑containing protein 66 in salivary adenoid cystic carcinoma.
Article in Oncology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 5 citations in OpenAlex.
- Role of WDR66 in Stemness, Therapy Resistance and Tumor microenvironment modulation in Head and Neck Cancer.International journal of biological sciences · 2026Article
- Molecular Aspects of Mucoepidermoid Carcinoma and Adenoid Cystic Carcinoma of the Salivary Gland.Head and neck pathology · 2024Review
- LncRNA HCG18 Promotes Osteosarcoma Cells Proliferation, Migration, and Invasion in by Regulating miR-34a/RUNX2 Pathway.Biochemical genetics · 2023Article
- Altered polymerase theta expression promotes chromosomal instability in salivary adenoid cystic carcinoma.Journal of cellular and molecular medicine · 2022Article
- Transcriptomic Biomarker Signatures for Discrimination of Oral Cancer Surgical Margins.Biomolecules · 2022Article
- PTEN Deregulation Mechanisms in Salivary Gland Carcinomas.Cancer diagnosis & prognosisReview
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Salivary adenoid cystic carcinoma (SACC) is one of the most common types of salivary gland cancer that causes substantial morbidity and mortality. Despite the substantial health burden of SACC, the molecular mechanisms underlying its development and progression remain poorly understood. We previously reported the loss of phosphatase and tensin homolog (PTEN) expression to be common among SACC tumors, and the PTEN deficiency to be correlated with enrichment of epithelial‑mesenchymal transition (EMT) genes based on expression array analysis. The aim of the present study was to investigate further the functional function of WD repeat‑containing protein 66 (WDR66), one of the enriched EMT genes, in the context of PTEN deficiency and SACC pathogenesis. WDR66 was identified to be required to maintain the EMT phenotype and the expression of cancer stem cell genes in the context of PTEN deficiency. Furthermore, knockdown of WDR66 decreased cellular proliferation, migration and invasion. Finally, WDR66 expression was identified to be inversely associated with PTEN expression and negatively correlated with the overall survival of patients with SACC. Collectively, the results of the present study revealed a novel function of WDR66 in mediating the progression of PTEN‑deficient SACCs, thereby suggesting WDR66 inhibition to be a potential therapeutic approach towards successful management of SACC disease progression, particularly against tumors with decreased PTEN expression levels.
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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.