Cancer-associated fibroblast-derived COL17A1 promotes gemcitabine resistance and tumorigenesis in pancreatic cancer cells by interacting with ACTN4.

ABSTRACT:

Background

Cancer-associated fibroblasts (CAFs) are key components of tumor microenvironment and have been identified to be involved in modulating drug resistance in cancers by secreting molecules. Pancreatic cancer (PC) is a leading cause of cancer mortality with high aggressiveness. Gemcitabine (GEM) is one of primary antineoplastic drugs for PC. Collagen XVII (COL17A1) expression was found to be upregulated in GEM-resistant CAFs. Here, this study focused on investigating whether CAFs affected GEM resistance in PC by secreting COL17A1 and its associated mechanisms.

Methods

In total, 60 newly diagnosed PC patients only with GEM-based chemotherapy were recruited. Normal fibroblasts (NFs) and CAFs were isolated using fresh normal and resistant PC tissues. Human pancreatic duc

SUBMITTER: Shi R 

PROVIDER: S-EPMC11799490 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature