Fig. 1: SETD1A is required for GC cell proliferation. | Cell Death & Disease

Fig. 1: SETD1A is required for GC cell proliferation.

From: Non-catalytic role of SETD1A promotes gastric cancer cell proliferation through the E2F4–TAF6 axis in the cell cycle

Fig. 1

A SETD1A mRNA expression in clinical GC subtypes from the TCGA dataset. NT, normal tissue, n = 36; MSI microsatellite instability, n = 72; GS genomically stable, n = 49; CIN chromosomal instability, n = 220; EBV Epstein–Barr virus, n = 30. B Kaplan–Meier survival analysis of patients with SETD1A-high vs SETD1A-low GC (n = 875). C Flag-tagged Cas9 expression in iCas9-AGS cells with or without 24 h of Dox treatment. D Western blotting quantification of SETD1A protein levels after 6 days of Dox treatment of sgRNA-expressing iCas9-AGS cells. E Competitive growth assay of sgRNA-expressing iCas9-AGS cells after Dox treatment. Results are presented as mean ± SD from three biological replicates. Asterisks indicate statistical significance compared with sgEmpty at each time point. F Cell cycle analysis via EdU incorporation at indicated time points in sgRNA-expressing iCas9-AGS cells. Results are presented as mean ± SD from three biological replicates. G Apoptosis was measured using Annexin V/7AAD staining at the indicated time points in sgRNA-expressing iCas9-AGS cells. Results are presented as mean ± SD from three biological replicates. H Alteration ratios of G1 phase, S phase, and apoptotic cells in sgSETD1A vs sgEmpty controls. Results are presented as mean ± SD from three biological replicates. Asterisks indicate statistical significance compared with day 0. I Western blotting results of G1 arrest markers after 6 days of Dox treatment. Representative images of three biological replicates are shown.

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