https://orcid.org/0000-0003-0270-1700
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Abstract
Aims: To explore the pathways and target genes related to N6-methyladenosine (m6A) methylation in ovarian cancer and their effect on patient prognosis. Methods & materials: The Cancer Genome Atlas was used to screen genes related to m6A regulators in terms of gene expression, mutation and copy number variation. These genes were subjected to pathway enrichment analysis. Prognosis-related genes were screened and involved in risk signature construction. Immunohistochemistry was used for verification. Results: We obtained 1408 genes dysregulated in parallel to m6A regulators, which were mainly involved in the platelet activation pathway. The m6A-related signature was constructed based on the expression of four prognosis-related genes (RPS6KA2, JUNB, HNF4A and P2RX1). Conclusion: This work provides new insights into the mechanism of m6A methylation in ovarian cancer.
Lay abstract
N6-methyladenosine (m6A) methylation is the most common type of modification on mRNA. m6A methylation can affect the biological function of cells by affecting the protein expression level of mRNA. The process of m6A modification is controlled by many m6A regulators, which are dysregulated in ovarian cancer. Our research aims to screen the genes that are related to m6A regulation to analyze targets and mechanisms in ovarian cancer. We screened 1408 m6A-related genes, which are mainly involved in the platelet activation pathway. Among them, RPS6KA2 and JUNB were significantly related to poor prognosis of patients with ovarian cancer. RPS6KA2 was positively correlated with the m6A regulator METTL3 in ovarian cancer. Our study provides a basis for future mechanism studies.
Supplementary data
To view the supplementary data that accompany this paper please visit the journal website at: www.tandfonline.com/doi/suppl/10.2217/epi-2021-0204
Acknowledgments
L Zhu, H Xu and X Li designed research. H Xu and X Li wrote manuscript. H Xu performed immunohistochemistry assay. X Li, H Xu, S Wang, F Li and L Yan involved in data collection and data statistical analysis. Li Zhu provided fund support and critically reviewed the manuscript. All authors read and approved the final manuscript.
Financial & competing interests disclosure
The present study was supported by grants from National Natural Science Foundation of China Youth Science Foundation (no. 81602438) and 345 Talent Project of Shengjing Hospital. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.
Ethical conduct of research
The studies involving human participants were reviewed and approved by the Clinical Research Ethics Committee of Shengjing Hospital of China Medical University (no. 2021PS485K). The authors have followed the principles outlined in the Declaration of Helsinki for all human or animal experimental investigations. In addition, for investigations involving human subjects, informed consent has been obtained from the participants involved.
Data sharing statement
The datasets analyzed during the current study are available in the UCSC Xena (https://xenabrowser.net), TCGA GDC (https://portal.gdc.cancer.gov), GEO (https://www.ncbi.nlm.nih.gov/geo/), CCLE (https://portals.broadinstitute.org/ccle) and GDSC (https://www.cancerrxgene.org) databases. All data generated during this study are included in this published article and its supplementary information files.