ArticleMedical oncology (Northwood, London, England)2020
Hypomethylated SPANXA1/A2 promotes the metastasis of head and neck squamous cell carcinoma.
Article in Medical oncology (Northwood, London, England), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- De Novo Genes: Current Status and Future Goals.Genome biology and evolution · 2025Article
- RMND5A upregulation via IGF2BP3-mediated mHuman cell · 2025Article
- Gene Expression Profiles of Methyltransferases and Demethylases Associated with Metastasis, Tumor Invasion, CpG73 Methylation, and HPV Status in Head and Neck Squamous Cell Carcinoma.Current issues in molecular biology · 2023Article
- Iodine nutrition and papillary thyroid cancer.Frontiers in nutrition · 2022Review
- Hypomethylation-driven AKT Serine/Threonine Kinase 3 promotes testicular germ cell tumors proliferation and negatively correlates to immune infiltration.Bioengineered · 2021Article
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Authors and funding
7 authors.
Funding
Abstract
The aberrant expression of SPANXA1/A2 (sperm protein associated with the nucleus on the X-chromosome, family members A1/A2) has been observed in multi types of cancers. However, the roles of SPANXA1/A2 in head and neck squamous cell carcinoma (HNSCC) remain largely unknown. The expression of SPANXA1/A2 was evaluated via analyzing UCSC XENA and GEO databases. To dissect the underlying cause of silencing SPANXA1/A2-mediated suppression, cell migration and invasion were detected in SPANXA1/A2 manipulated cell lines. Western blot was performed to evaluate EMT-related factors. The methylation microarray data of SPANXA1/A2 in HNSCC from the UCSC XENA database were used to identify whether aberrant overexpressed SPANXA1/A2 is induced by aberrant DNA methylation. SPANXA1/A2 was highly expressed in tumor tissues and associated with poor survival of patients with HNSCC. Knockdown of SPANXA1/A2 inhibited migration and invasion abilities in both Cal-27 and SCC-9 cells through epithelial-mesenchymal transition (EMT) suppression. The SPANXA1/A2 expression negatively related to its DNA methylation level. SPANXA1/A2 DNA hypomethylation was associated with metastatic stage and poor survival of patients with HNSCC. A dose-dependent increase of SPANXA1/A2 mRNA was observed in both cal-27 and SCC-9 cells after treatment with 5-AZA-2'-deoxycytidine (5-AZA-CdR). We demonstrated that knockdown of SPANXA1/A2 obviously inhibited tumor cell migration and invasion through EMT suppression. DNA hypomethylation might be responsible for the aberrant SPANXA1/A2 overexpressing. SPANXA1/A2 may be used as a diagnosed and independent prognosis indicator of HNSCC, and knockdown of SPANXA1/A2 may present a new gene-based therapy for HNSCC.
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