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. Author manuscript; available in PMC: 2022 Sep 1.
Published in final edited form as: Cancer Res. 2022 Mar 1;82(5):900–915. doi: 10.1158/0008-5472.CAN-20-0948

Figure 2. Delivery of ASO1-cEt/DNA by free uptake induces PKM splice switching in Huh7 cells.

Figure 2.

(A) ASO1-cEt/DNA induces PKM splice switching in a dose-dependent manner. Radioactive RT-PCR analysis after treating Huh7 cells with varying ASO concentrations by free uptake for four days. (B) Quantification of PKM1 and PKMds isoforms in panel (A). (C) Radioactive RT-PCR analysis after treating Huh7 cells with 20 μM ASO by free uptake for 7 days. Medium and ASO were replenished on day 4. (D) Quantification of PKM1 and PKMds isoforms in panel (C). (E) RT-qPCR quantitation of the indicated transcripts upon ASO treatment as in panel (C). All tested transcripts were normalized to the HPRT transcript level. Relative expression versus the NTC is shown. (F) Western blotting analysis of the PKM isoform switch after treating Huh7 cells with ASO as in panel (C), with quantification of band intensities shown below; bands were normalized to tubulin and to the NTC. The bar charts in panels (B and D) represent the average of three independent biological replicates ± SEM. One-way ANOVA was performed with Dunnett’s multiple comparison post-hoc test. * P ≤ 0.05; ** P ≤ 0.01; *** P ≤ 0.001.