The interplay between N6-methyladenosine (m6A) modification and microRNAs (miRs) participates in cancer progression. This study is conducted to explore the role of miR-19a-3p in nasopharyngeal carcinoma (NPC) cell proliferation and invasion. RT-qPCR and western blot showed that miR-19a-3p was upregulated in NPC tissues and cells and related to poor prognosis, methyltransferase-like 3 (METTL3) was highly expressed while BMP and activin membrane-bound inhibitor (BAMBI) was weakly expressed in NPC tissues and cells. miR-19a-3p downregulation inhibited cell proliferation and invasion while miR-19a-3p overexpression played an opposite role. m6A quantification and m6A RNA immunoprecipitation assays showed that METTL3-mediated m6A modification promoted the processing and maturation of pri-miR-19a via DGCR8. Dual-luciferase assay showed that BAMBI was a target of miR-19a-3p. The rescue experiments showed that BAMBI downregulation reversed the role of miR-19a-3p inhibition in NPC cells. A xenograft tumor model showed that METTL3 downregulation inhibited tumor growth via the miR-19a-3p/BAMBI in vivo. Overall, our findings elicited that METTL3-mediated m6A modification facilitated the processing and maturation of pri-miR-19a via DGCR8 to upregulate miR-19a-3p, and miR-19a-3p inhibited BAMBI expression to promote NPC cell proliferation and invasion, thus driving NPC progression.

Currently, FTH1 has been increasingly found to play a crucial role in cancer as a core regulator of ferroptosis, while its role of non-ferroptosis in HNSCC is still unclear. Herein, we analyzed the expression level of FTH1 in HNSCC using TCGA database and FTH1 protein in HNSCC tissues and cell lines was determined by immunohistochemistry (IHC) and western blotting, respectively. Then, its prognostic value and relationship with clinical parameters were investigated in HNSCC patients. Additionally, the biological function and its molecular mechanism of FTH1 in HNSCC were explored. The current study showed that FTH1 is significantly overexpressed in HNSCC tissues and related to poor prognosis and lymph node metastasis of HNSCC. FTH1 knockdown could suppress the metastasis and epithelial-mesenchymal transition (EMT) process of HNSCC and we further demonstrated that it may be caused by the inactivation of β-catenin/ZEB1 through HMOX1. Taken together, our findings indicate that FTH1 plays a critical role in the progression and metastasis of HNSCC and can serve as a promising prognostic factor and therapeutic target in HNSCC.