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As a crucial anti\u2010tumour agent with explicit toxicity, cisplatin may render resistance through intertwined mechanisms, even in disease entities with high curative ratio, such as seminoma. Previously, we established cisplatin\u2010resistant seminoma TCam\u20102 (TCam\u20102\/CDDP) cells and showed that epigenetic regulations, such as non\u2010coding RNA (ncRNA) interactions, might orchestrate cell fate decisions in the cisplatin treatment context in seminoma. N6\u2010methyladenosine (m6A) is the most prevalent internal modification in mRNA. In the present study, we assessed cisplatin resistance in seminoma from the perspective of m\n                    <jats:sup>6<\/jats:sup>\n                    A, another manner of epigenetic modification. The global m\n                    <jats:sup>6<\/jats:sup>\n                    A enrichment of TCam\u20102 and TCam\u20102\/CDDP was depicted. Then, we elucidated whether transcription factor\u2010activating enhancer\u2010binding protein 2C (TFAP2C) was functionally m\n                    <jats:sup>6<\/jats:sup>\n                    A\u2010modified by methyltransferase\u2010like protein 3 (METTL3), which acted as an m\n                    <jats:sup>6<\/jats:sup>\n                    A \u2018writer\u2019, and insulin\u2010like growth factor 2 mRNA\u2010binding protein 1 (IGF2BP1), which acted as an m\n                    <jats:sup>6<\/jats:sup>\n                    A \u2018reader\u2019. Enhanced stability of TFAP2C mRNA promoted seminoma cell survival under cisplatin treatment burden probably through up\u2010regulation of DNA repair\u2010related genes. Hopefully, this study will help improve our understanding of the subtleties of the tumour cellular coping strategy in response to chemotherapy. Targeting factors that are involved in m\n                    <jats:sup>6<\/jats:sup>\n                    A methylation may be an effective strategy for circumventing cisplatin resistance in seminoma.\n                  <\/jats:p>","DOI":"10.1111\/jcmm.15738","type":"journal-article","created":{"date-parts":[[2020,8,28]],"date-time":"2020-08-28T18:45:00Z","timestamp":1598640300000},"page":"11366-11380","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":57,"title":["METTL3 potentiates resistance to cisplatin through m\n                    <sup>6<\/sup>\n                    A modification of TFAP2C in seminoma"],"prefix":"10.1111","volume":"24","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1037-7990","authenticated-orcid":false,"given":"Jingchao","family":"Wei","sequence":"first","affiliation":[{"name":"Department of Urology The Second Affiliated Hospital of Zhejiang University School of Medicine Hangzhou 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