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Abstract
N6-methyladenosine (m6A) is the most common post-transcriptional modification of RNA in eukaryotes, which has been demonstrated to play important roles in various cancers. YTHDF1 acts as a crucial m6A “reader” and regulates the fate of m6A modified mRNA. However, its role in cervical cancer remains unknown. In this study, we showed that YTHDF1 was highly expressed in cervical cancer, and was closely associated with the poor prognosis of cervical cancer patients. YTHDF1 knockdown suppressed the growth, migration and invasion, and induced apoptosis of cervical cancer cells. Moreover, YTHDF1 knockdown inhibited tumorigenesis of cervical cancer cells in vivo. Through combined on-line data analysis of RIP-seq, meRIP-seq and Ribo-seq upon YTHDF1 knockdown, RANBP2 was identified as the key target of YTHDF1 in cervical cancer cells. YTHDF1 regulated RANBP2 translation in an m6A-dependent manner without effect on its mRNA expression. RANBP2 potentiated the growth, migration and invasion of cervical cancer cells. Our study demonstrated the oncogenic role of YTHDF1 in cervical cancer by regulating RANBP2 expression and YTHDF1 represents a potential target for cervical cancer therapy.
Highlights
Cervical cancer (CC) is one of the most common malignant tumors among female patients, which mortality rate ranks fourth in the world [1]
METTL3 activates the oncogene c-MYC by enhancing the m6A modification of SP1 [13], it promotes the translation of BCL2 and PTEN mRNA through the up-regulation of their m6A modification [14], which leads to the development of acute myeloid leukemia (AML)
Results showed that the expression of several m6A regulators was changed in cervical cancer, among which YTHDF1 expression was increased most significantly (Figure 1A)
Summary
Cervical cancer (CC) is one of the most common malignant tumors among female patients, which mortality rate ranks fourth in the world [1]. Increasing studies have shown that the m6A regulators including m6A “writers”, “erasers” and “readers” are dysregulated in YTHDF1 Promotes Cervical Cancer Progression multiple cancers and play an important role in tumor cell proliferation, differentiation arrest, survival, tumorigenesis and metastasis [12]. FTO promotes cancer cell proliferation and metastasis through negative regulation of BNIP3 mRNA, and the high level of FTO is associated with the poor prognosis [17]. YTHDF1 promotes the epithelial-mesenchymal transition (EMT) of liver cancer cells by regulating the translation of Snail mRNA [20]. YTHDF1 is upregulated in human colon cancer tissues, which predicts the poor prognosis of colon cancer patients [22]
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