The m6A reader HNRNPC promotes glioma progression by enhancing the stability of IRAK1 mRNA through the MAPK pathway
Glioma is the most common and aggressive primary malignant brain tumor. N6-methyladenosine (m6A) modification widely exists in eukaryotic cells and plays an important role in the occurrence and development of human tumors. Here, we show that the m6A reader HNRNPC was overexpression and related to poor prognosis in glioma patients. HNRNPC plays crucial role in glioma cell proliferation, invasion and tumorigenesis. HNRNPC augments m6A-dependent mRNA stability of IRAK1, which impacted poor survival for glioma patients, further activated the downstream MAPK pathway. HNRNPC promotes glioma cells progression largely through the upregulation of IRAK1. Together, our findings demonstrate the novel HNRNPC-IRAK1-MAPK axis critical for glioma tumorigenesis and extend the reason for the upregulation of IRAK1. Overall design: To investigate the mechanism whereby HNRNPC affects the malignant behavior of gliomas, we performed RNA-seq on the U251 cell line after HNRNPC knockdown by siRNA.