Observational analysis shows collagen XVII enhances tumor growth via PIK3R5 regulation in pancreatic ductal adenocarcinoma, implying a potential therapeutic target.
The expression of PIK3R5 and activation of AKT is dependent on collagen XVII. A, Bubble plots illustrating two upregulated gene ontology programs in collagen XVII–deficient MGH1275 cells. B, Volcano plot showing DEGs in tumors formed by MGH1275 cells expressing an NTC vector vs. COL17A1-specific shRNAs. C, Relative expression of PIK3R5 in tumors formed by MGH1319 cells expressing an NTC shRNA and COL17A1-specific shRNAs. The mean (±SEM) from three tumors analyzed in triplicate is shown. ***, P < 0.001, one-way ANOVA with Dunnett’s post hoc test. D, IHC staining of PIK3R5, P-AKT, and total AKT on orthotopic tumors formed by MGH1319 and MGH1275 cells expressing an NTC vector or COL17A1-specific shRNAs. Scale bars, 100 and 25 µm (inset). FDR q value, Fasle Discovery Rate-adjusted q-value; NES, normalized enrichment scale; NOM_P value, nominal P-value.
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Hank et al. (2025) studied this question.
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