METTL14 Inhibits Hepatocellular Carcinoma Metastasis Through Regulating EGFR/PI3K/AKT Signaling Pathway in an m6A-Dependent Manner.

摘要: Purpose Hepatocellular carcinoma (HCC) ranks as the fourth leading cause of cancer-related deaths worldwide. N6-methyladenosine (m6A) RNA methylation is most common modification messenger RNAs (mRNAs). The prognosis HCC patients with metastasis remains poor. Our study aimed to elucidate regulatory role m6A on metastasis. Patients and methods All were enrolled from Affiliated Huai'an No. 1 People's Hospital Nanjing Medical University. expression levels gene tested by quantitative polymerase chain reaction (qPCR), Western blot, or immunohistochemistry (IHC) analysis. Wound healing assay, Transwell invasion lung model implemented investigate migration ability cells. Candidate targets selected a comprehensive analysis RNA-sequencing m6A-sequencing HepG2 Results In this study, we demonstrated that METTL14 was significantly downregulated in associated patients. knockdown promoted migration, invasion, epithelial-mesenchymal transition (EMT) cells vitro vivo. addition, overlapping data, identified EGFR direct target HCC. Mechanistically, found inhibit cell EMT through modulating EGFR/PI3K/AKT signaling pathway an m6A-dependent manner. Conclusion Targeting METTL14/EGFR/PI3K/AKT may facilitate development new treatment strategy against