The FN1 Knockout PANC-1 Cell Line is a CRISPR/Cas9-edited knockout cell line generated from the PANC-1 pancreatic ductal adenocarcinoma epithelial cell line. Designed as a loss-of-function model, this product allows researchers to investigate the biological roles of fibronectin, a key extracellular matrix (ECM) glycoprotein encoded by the FN1 gene, through CRISPR/Cas9-mediated gene disruption. The cell line provides a genetically defined system to dissect fibronectin-dependent processes in a human pancreatic cancer background, particularly for studying integrin-mediated adhesion and signaling pathways.
PANC-1 is an adherent epithelial cell line derived from a male patient with pancreatic ductal adenocarcinoma. It harbors activating mutations in KRAS and TP53, two of the most prevalent genetic alterations in pancreatic cancer, making it a standard model for studying tumor progression, metastasis, and drug response. PANC-1 cells are characterized by their polygonal morphology and ability to form tumors in vivo, making them a reliable platform for functional genomics studies. The cell line retains characteristic features of pancreatic cancer cells, including aggressive growth and metastatic potential, and is widely used in preclinical oncology research.
Fibronectin is a multifunctional ECM glycoprotein that mediates cell adhesion, migration, and wound healing by binding to integrin receptors such as ??5??1 and ??V??3. Ligand-bound integrins activate focal adhesion kinase (FAK) and Src, which propagate signals through the PI3K-Akt and MAPK/ERK cascades, as well as the small GTPase Rac1. FN1 transcription is upregulated by TGF-??, EGF, PDGF, and hypoxia-inducible factor 1 (HIF-1) in response to mechanical stress and tissue remodeling. Downstream, fibronectin signaling modulates effectors including ERK1/2, Akt, RhoA, MMP-2/9, and cyclin D1. Fibronectin also interacts with collagens, heparin, fibrin, VEGF, and cytoskeletal adaptors talin and vinculin, positioning it at the center of focal adhesion and ECM-receptor interaction networks.
In the PANC-1 context, FN1 knockout abrogates fibronectin expression and disrupts integrin-mediated adhesion, leading to attenuated cell migration, invasion, and metastatic capability. Loss of fibronectin can alter sensitivity to chemotherapeutic agents and reduce anoikis resistance, processes critical for cancer dissemination. This abrogation also affects downstream signaling events such as FAK and Akt phosphorylation, which are critical for survival and motility. This knockout model therefore provides a powerful tool to explore how ECM components influence the aggressive behavior of KRAS/TP53-mutant pancreatic cancer cells and to study mechanisms of ECM-dependent tumor progression and drug resistance.
This product is applicable across a range of experimental settings including pancreatic cancer metastasis research, ECM remodeling studies, and tumor microenvironment investigations. Researchers can perform Western blotting for fibronectin, RT-qPCR for FN1 mRNA, immunofluorescence of ECM components, Transwell migration/invasion assays, adhesion and anoikis assays, phospho-signaling analyses (e.g., pFAK, pAKT), co-immunoprecipitation of integrin complexes, and transcriptomic profiling via RNA-seq. The knockout cell line supports studies on chemoresistance, wound healing, and fibrosis modulation. For more information, please contact Ascent Research.
