What type of study is this?

This is a In Vitro Study study (also classified as: Animal Study, Observational).

August 17, 2025

Figure 6 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5

Key Points

Collagen XVII promotes pancreatic ductal adenocarcinoma tumor growth through PIK3R5 regulation, enhancing AKT activation.
Significant upregulation of PIK3R5 was observed in tumors derived from collagen XVII-deficient cells, P < 0.001.
Analysis involved comparing gene expression in tumors using COL17A1-specific shRNAs against control vectors, highlighting regulation pathways.
Results indicate potential therapeutic implications for targeting collagen XVII in pancreatic ductal adenocarcinoma management.

Abstract

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 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; NOMP value, nominal P-value.

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