科研之友
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摘要
Aims: N6-Methyladenosine (m(6)A) is the most frequent posttranscriptional modification and plays important roles in tumorigenesis and metastasis. The roles of fat mass and obesity-associated (FTO) in metabolic diseases have been widely explored. However, the molecular mechanisms and physiological functions of FTO in prostate cancer remain largely unknown. This study aimed to explore the exact functions of FTO in the progression of prostate cancer metastasis. @@@ Main methods: Dot blot and m(6)A RNA methylation quantification assays were performed to determine m(6)A levels. The protein and mRNA expression levels were detected using immunoblot (IB) and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analyses. Cell invasion and migration abilities were measured using transwell and wound healing assays. Bioinformatics was used to measure the expression level of FTO and possible correlation between FTO levels and advanced tumor stage. Immunofluorescence (IF) was performed to measure the cellular localization of FTO. @@@ Key findings: FTO was downregulated in prostate cancer tissues and cell lines, and the m(6)A content was increased. Importantly, patients with lower FTO expression had advanced tumor stage and higher Gleason scores. Gain- and loss-of-function assays revealed that FTO inhibits prostate cancer cell invasion and migration in vitro. Moreover, we confirmed that FTO can decrease the total m(6)A level. @@@ Significance: The present study revealed that the FTO m(6)A demethylase inhibits prostate cancer cell invasion and migration by regulating total m(6)A levels.
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单位y; 南方医科大学
