Abstract
Ankyrin repeat domain protein 22 (ANKRD22) has been implicated in various types of cancers but its expression and potential functions have not been investigated in gliomas. In this study, the high expression of ANKRD22 in gliomas and its correlation with survival were identified based on the Cancer Genome Atlas database. Similar expression trends were observed in glioma tissues and cell lines. Functionally, the loss of ANKRD22 suppressed glioma cell proliferation, migration, and invasion and cell cycle progression in vitro and tumor growth in vivo. Mechanistically, ANKRD22 interacted with the E2F transcription factor 1 (E2F1), thereby upregulating maternal embryonic leucine zipper kinase (MELK) protein expression. Moreover, E2F1 overexpression partly restored ANKRD22 silence-mediated tumor suppressive effects in glioma cells. In conclusion, our data highlight the oncogenic role of ANKRD22 in gliomas via E2F1/MELK signaling, which may serve as a promising target for glioma treatment.
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