METTL3 promotes translation in human cancer cells. METTL3 is an RNA methyltransferase involved in mRNA biogenesis, decay, and translation control through N⁶-methyladenosine (m⁶A) modification. This study shows that METTL3 enhances the translation of specific mRNAs, including the epidermal growth factor receptor (EGFR) and the Hippo pathway effector TAZ, in human cancer cells. Unlike previous models that suggest METTL3 acts through downstream m⁶A reader proteins, this research demonstrates that METTL3 associates with ribosomes and promotes translation in the cytoplasm. METTL3 depletion inhibits translation, and both wild-type and catalytically inactive METTL3 promote translation when tethered to a reporter mRNA. Mechanistically, METTL3 enhances mRNA translation through interaction with the translation initiation machinery. METTL3 expression is elevated in lung adenocarcinoma, and both loss- and gain-of-function studies show that METTL3 promotes the growth, survival, and invasion of human lung cancer cells. These findings highlight an important role of METTL3 in promoting the translation of oncogenes in human lung cancer. The study also reveals that METTL3 enhances translation of target mRNAs by recruiting eIF3 to the translation initiation complex. METTL3 promotes cancer cell growth, survival, and invasion, suggesting it could be a potential target for cancer therapy. The results indicate that METTL3 plays a direct role in promoting translation, independent of its methyltransferase activity or downstream m⁶A reader proteins.METTL3 promotes translation in human cancer cells. METTL3 is an RNA methyltransferase involved in mRNA biogenesis, decay, and translation control through N⁶-methyladenosine (m⁶A) modification. This study shows that METTL3 enhances the translation of specific mRNAs, including the epidermal growth factor receptor (EGFR) and the Hippo pathway effector TAZ, in human cancer cells. Unlike previous models that suggest METTL3 acts through downstream m⁶A reader proteins, this research demonstrates that METTL3 associates with ribosomes and promotes translation in the cytoplasm. METTL3 depletion inhibits translation, and both wild-type and catalytically inactive METTL3 promote translation when tethered to a reporter mRNA. Mechanistically, METTL3 enhances mRNA translation through interaction with the translation initiation machinery. METTL3 expression is elevated in lung adenocarcinoma, and both loss- and gain-of-function studies show that METTL3 promotes the growth, survival, and invasion of human lung cancer cells. These findings highlight an important role of METTL3 in promoting the translation of oncogenes in human lung cancer. The study also reveals that METTL3 enhances translation of target mRNAs by recruiting eIF3 to the translation initiation complex. METTL3 promotes cancer cell growth, survival, and invasion, suggesting it could be a potential target for cancer therapy. The results indicate that METTL3 plays a direct role in promoting translation, independent of its methyltransferase activity or downstream m⁶A reader proteins.