期刊
FRONTIERS IN ONCOLOGY
卷 11, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fonc.2021.734655
关键词
CDCA7; cell cycle; CCNA2; copy number amplification; ESCC (esophageal squamous cell carcinoma)
类别
资金
- National Natural Science Foundation of China [81602175, 81773150, 81972613]
- Fund for Shanxi 1331 Project
- 1331 Project Key Subjects Construction
- Fund for Sanjin Scholars
- Foundation for Youths of Shanxi Province [201901D211349, 201901D211345]
- Natural Science Foundation of Shanxi Province [201801D121306]
The study revealed that CDCA7 may act as an oncogene by directly upregulating CCNA2 to facilitate tumor progression in ESCC.
Background CDCA7 is a copy number amplified gene identified not only in esophageal squamous cell carcinoma (ESCC) but also in various cancer types. Its clinical relevance and underlying mechanisms in ESCC have remained unknown. Methods Tissue microarray data was used to analyze its expression in 179 ESCC samples. The effects of CDCA7 on proliferation, colony formation, and cell cycle were tested in ESCC cells. Real-time PCR and Western blot were used to detect the expression of its target genes. Correlation of CDCA7 with its target genes in ESCC and various SCC types was analyzed using GSE53625 and TCGA data. The mechanism of CDCA7 was studied by chromatin immunoprecipitation (ChIP), luciferase reporter assays, and rescue assay. Results The overexpression of CDCA7 promoted proliferation, colony formation, and cell cycle in ESCC cells. CDCA7 affected the expression of cyclins in different cell phases. GSE53625 and TCGA data showed CCNA2 expression was positively correlated with CDCA7. The knockdown of CCNA2 reversed the malignant phenotype induced by CDCA7 overexpression. Furthermore, CDCA7 was found to directly bind to CCNA2, thus promoting its expression. Conclusions Our results reveal a novel mechanism of CDCA7 that it may act as an oncogene by directly upregulating CCNA2 to facilitate tumor progression in ESCC.
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