RETRACTED ARTICLE: CircRNA circ-ATAD1 is downregulated in endometrial cancer and suppresses cell invasion and migration by downregulating miR-10a through methylation

It has been reported that circ-ATAD1 promotes the development of gastric cancer. This study was carried out to analyze the role of circ-ATAD1 in endometrial cancer (EC). EC and paired non-tumor tissues from EC patients ( n  = 60) were subjected to the isolation of total RNA and RT-qPCR to analyze th...

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Bibliographic Details
Published in:Mammalian genome 2021-12, Vol.32 (6), p.488-494
Main Authors: Yang, Pengxia, Yun, Kunlun, Zhang, Ruying
Format: Article
Language:English
Subjects:
Animal Genetics and Genomics
Biomedical and Life Sciences
Cell Biology
Cell migration
DNA methylation
Endometrial cancer
Endometrium
Gastric cancer
Human Genetics
Life Sciences
Tumors
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Summary:It has been reported that circ-ATAD1 promotes the development of gastric cancer. This study was carried out to analyze the role of circ-ATAD1 in endometrial cancer (EC). EC and paired non-tumor tissues from EC patients ( n  = 60) were subjected to the isolation of total RNA and RT-qPCR to analyze the expression of circ-ATAD1 and miR-10a. Correlations between circ-ATAD1 and miR-10a were analyzed by Pearson’s correlation coefficient. The effects of circ-ATAD1 overexpression on miR-10a expression and methylation were analyzed by RT-qPCR and methylation-specific PCR (MSP). The roles of circ-ATAD1 and miR-10a in regulating EC cell invasion and migration were analyzed by Transwell assays. We found that circ-ATAD1 was downregulated in EC, while miR-10a was upregulated in EC. An inverse correlation between circ-ATAD1 and miR-10a was observed across EC samples. In EC cells, circ-ATAD1 overexpression decreased miR-10a expression and increased miR-10a gene methylation. Transwell assay analysis showed that circ-ATAD1 overexpression totally reversed the enhancing effects of miR-10a on EC cell invasion and migration. Circ-ATAD1 is downregulated in EC and may suppress EC cell invasion and migration by downregulating miR-10a through methylation.
ISSN:0938-8990
1432-1777
DOI:10.1007/s00335-021-09899-9