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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 1. Delivery of ASO1-cEt/DNA via lipofectamine induces PKM splice switching in Huh7 cells.

Figure 1.

(A) Radioactive RT-PCR shows the extent of PKM splice-switching after transfecting Huh7 cells with 60 nM ASO for two days. No-treatment control (NTC) with or without reverse transcriptase (+ RT or − RT, respectively) and a control ASO (Ctrl-cEt/DNA) with 5mismatch nucleotides to PKM exon 10 were used as controls. (B) Quantification of PKM1 and PKMds isoforms in panel (A). (C) RT-qPCR quantitation of the indicated transcripts upon ASO treatment as in panel (A). All tested transcripts were normalized to the HPRT transcript level. Relative expression to the NTC is presented. (D) Western blotting analysis of the PKM isoform switch after ASO treatment as in panel (A), with quantification of band intensities shown below; bands were normalized to tubulin and to the NTC The bar charts in panel (B and C) represent the average of three independent biological replicates ± SEM. One-way ANOVA was performed with Dunnett’s multiple comparison post-hoc test. ** P ≤ 0.01; *** P ≤ 0.001.