ATXN2-Mediated PI3K/AKT Activation Confers Gastric Cancer Chemoresistance and Attenuates CD8⁺ T Cell Cytotoxicity

Figure 3

ATXN2 activated the PI3K/AKT pathway. (a) Heatmap of altered genes when ATXN2 was downregulated in SGC7901/5-FU cells. (b) KEGG pathway analysis of changed pathways when ATXN2 was downregulated in SGC7901/5-FU cells. (c) Phosphorylation levels of PI3K and AKT were measured by Western blot. (d) Protein levels of p-AKT and AKT in SGC7901 cells overexpressing ATXN2 or treated with an AKT inhibitor. (e) Apoptosis rates of SGC7901 cells overexpressing ATXN2 or treated with an AKT inhibitor were detected after treatment with 5-FU (10 μg/mL). (f) Downregulated genes enriched in the PI3K/AKT pathway. (g) Protein level of BCL2L1 in SGC7901 cells and SGC7901/5-FU cells. (h) Protein level of BCL2L1 in SGC7901 cells overexpressing ATXN2 and/or silencing BCL2L1. (i) Apoptosis rates of SGC7901 cells overexpressing ATXN2 or (and) silencing BCL2L1 were detected after treatment with 5-FU (10 μg/mL). (j) The correlation between ATXN2, AKT, and BCL2L1 expression in the TCIA and GEPIA databases. .

(a)

(b)

(c)

(d)

(e)

(f)

(g)

(h)

(i)

(j)