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. Author manuscript; available in PMC: 2024 Feb 5.
Published in final edited form as: Cell Rep. 2023 Nov 18;42(12):113434. doi: 10.1016/j.celrep.2023.113434

Figure 4. SERPINB3 knockout and inhibition of MYC signaling abrogates the differentiation into the basal-like/squamous subtype of PDAC.

Figure 4.

(A–D) IPA (blue bars) and GSEA indicate similar pathway patterns following either treatment with a MYC inhibitor (10058-F4, 100 μM) (A and B) or SERPINB3 knockout (C and D), including enrichment of cellular movement and decreased basal-like/squamous differentiation, mirroring the observations made in SERPINB3-expressing PDAC cells as well as SERPINB3-high and basal-like/squamous PDAC tumors (Figure 2).

(E) SERPINB3 knockout decreases the ability of PDAC cells to invade. Cells that passed through a cell culture insert membrane coated with Matrigel were fixed, and the cells were counted. Data are presented as the mean ± SD of three independent experiments; *p < 0.05, **p < 0.01 by unpaired two-tailed Student’s t test.

(F) Calpain, a cysteine protease, is a key pathway for MYC degradation.32

(G) Calpain activity was reduced in the SERPINB3-overexpressing PDAC cell line (AsPC-1) but activated in SERPINB3-knockout PDAC cell lines (BxPC-3 and Panc 10.05). Data are presented as the mean ± SD (n = 4 for each group); **p < 0.01, ***p < 0.005 by unpaired two-tailed Student’s t test. IPA, Ingenuity pathway analysis; GSEA, gene set enrichment analysis. See also Figure S3.