TP53 and cervical carcinoma: Gene ontology (GO) analysis suggested that most downregulated genes upon knocking down FTO were enriched in cancer associated pathways, such as E2F1 targets, Epithelial mesenchymal transition (EMT), cell cycle regulation and glycolysis; in contrast, most upregulated genes were enriched in tumor suppressing pathways, including p53 pathway, unfolded protein response (UPR) and DNA damage repairs (Fig. 4b), these findings further supported the notion that FTO was a oncogenic factor contributed to cervical cancer progression.