期刊
MEDICAL ONCOLOGY
卷 37, 期 12, 页码 -出版社
HUMANA PRESS INC
DOI: 10.1007/s12032-020-01441-2
关键词
SPANXA1; A2; Head and neck squamous cell carcinoma (HNSCC); Migration and invasion; Epithelial– mesenchymal transition (EMT); TCGA
类别
资金
- National Natural Science Foundation of China [31472054, 81974297]
- National Key Research and Development Program of China [2016YFC1000600]
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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