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FTO promotes proliferation and migration of bladder cancer via enhancing stability of STAT3 mRNA in an m6A-dependent manner

N6-Methyladenosine (m6A) plays a key role in the occurrence and development of various cancers. Fat mass and obesity‐associated protein (FTO) was is involved in multiple cancers owing to its demethylase activity, and the molecular mechanism underlying FTO-promoted bladder cancer proliferation and mi...

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Detalles Bibliográficos
Autores principales: Sun, Zhuang, Sun, Xiaolu, Qin, Guoliang, Li, Yi, Zhou, Guanwen, Jiang, Xianzhou
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10405749/
https://www.ncbi.nlm.nih.gov/pubmed/37538000
http://dx.doi.org/10.1080/15592294.2023.2242688
Descripción
Sumario:N6-Methyladenosine (m6A) plays a key role in the occurrence and development of various cancers. Fat mass and obesity‐associated protein (FTO) was is involved in multiple cancers owing to its demethylase activity, and the molecular mechanism underlying FTO-promoted bladder cancer proliferation and migration via the regulation of RNA stability requires further investigation. In the present study, FTO was upregulated in bladder cancer and related to poor prognosis. Gain- and loss-of-function experiments showed that the upregulation of FTO promoted bladder cancer proliferation and migration. Mechanistic studies showed that FTO enhanced the stability of signal transducer and activator of transcription 3 (STAT3) mRNA in an m6A-dependent manner, thereby increasing STAT3 expression, which subsequently promoted P-STAT3 expression and activated STAT3 signalling pathway. Overall, this study revealed that the critical role of FTO in the progression of bladder cancer and could provide a novel avenue to regulate oncogene STAT3.