What type of study is this?

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

August 17, 2025

Figure 3 from Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5

Key Points

Collagen XVII promotes tumor growth in pancreatic ductal adenocarcinoma, highlighting its role in cancer progression.
Key evidence shows that collagen XVII expression is upregulated in PDAC cells upon interaction with cancer-associated fibroblasts.
Analysis of xenograft models revealed increased COL17A1 expression linked to tumor growth and CAF interaction.
These findings suggest that targeting collagen XVII and its pathways may lead to new therapeutic strategies in pancreatic cancer treatment.

Abstract

Collagen XVII expression is upregulated in PDAC cells upon interaction with CAFs. A, Western blot analysis of collagen XVII expression in immortalized human pancreatic ductal cells human pancreatic duct epithelial (HPDE), six PDAC cell lines, and telomerase reverse transcriptase–immortalized CAFs (CAF-1). β-Actin is shown as a loading control. B,COL17A1 expression in cell lines and matching xenograft tumors. C, Representative IHC staining of collagen XVII in cell line xenografts and PDXs of MGH1319. Scale bars, 50 μm. D, Schematic of the experimental setup of coculture and FACS of PDAC and CAF-1 cells. E, Collagen XVII expression in MGH1319 cells in monoculture and after coculture with CAF-1. β-Actin is shown as a loading control. F–H, Relative COL17A1 expression in MGH1319, MGH1275, MGH1108, and CAF-1 after mono- and coculture. The average (±SEM) from three independent experiments is shown. *, P P t test).

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