Fig. 8: A schematic model for NAF1 promoting glioma tumorigenesis and progression through enhancing ribosome biosynthesis. | Oncogenesis

Fig. 8: A schematic model for NAF1 promoting glioma tumorigenesis and progression through enhancing ribosome biosynthesis.

From: Increased expression of NAF1 contributes to malignant phenotypes of glioma cells through promoting protein synthesis and associates with poor patient survival

Fig. 8

NAF1 plays a crucial role in maintaining the yield of mature H/ACA RNPs. During malignant transformation of glioma cells, increased expression of NAF1 promotes U17 snoRNA processing, 18S rRNA maturation, and the assembly of 40 S subunits, thereby enhancing protein synthesis, including some key molecules associated with malignant progression of gliomas, such as c-Myc, NRF2, TERT, POLR1A, and POLR2A. Meanwhile, c-Myc, NRF2, and TERT in turn transcriptionally upregulate NAF1 expression, while POLR1A and POLR2A also can active the transcription of 45S rRNA, c-Myc, NRF2, TERT, and H/ACA snoRNA. These observations indicate that there exist positive feedback loops between NAF1 and these key molecules. In addition, NAF1 can maintain telomere length by increasing the levels of TERT and TERC at transcriptional or post-transcriptional levels. Altogether, these molecular events will contribute to glioma tumorigenesis and progression

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