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. Author manuscript; available in PMC: 2024 Sep 1.
Published in final edited form as: Wiley Interdiscip Rev RNA. 2023 Apr 11;14(5):e1788. doi: 10.1002/wrna.1788

Figure 4. HNRNPF/H proteins and the expression of cancer-specific transcripts.

Figure 4.

(A) Schematics of the mechanisms by which HNRNPF/H genes or proteins can contribute to tumorigenesis. Mechanisms shown are the HNRNPF/H-dependent processing of cancer-specific transcripts, the effect of mutations that disrupt HNRNPF/H protein expression or function or the binding sites of these proteins, and the involvement of HNRNPF/H genes in chromosomal translocations. (B) Schematic of the HNRNPH1-dependent exclusion of EWSR1-exon 8 present in the EWSR1::FLI1 transcripts expressed in a subset of the pediatric tumor Ewing sarcoma (see Grohar et al., 2016; Neckles et al., 2019; Vo et al., 2022) for further details). In vitro analysis has demonstrated that HNRNPH1 binds EWSR1-exon 8 G-rich sequences in non-G4 and G4 states, and that its binding favors accumulation of the bound RNA in an unfolded state (Vo et al., 2022). Figure panels created with BioRender.com.