The TM4SF1 Knockout PANC-1 Cell Line is a CRISPR/Cas9-edited knockout cell line in which the TM4SF1 gene has been disrupted to establish a loss-of-function model for studying the molecular mechanisms underlying pancreatic ductal adenocarcinoma. This engineered cell line is derived from the well-characterized PANC-1 parental line and offers a defined genetic background for interrogating TM4SF1-dependent signaling events. The knockout was generated using CRISPR/Cas9-mediated gene disruption, resulting in stable ablation of TM4SF1 expression, and serves as a critical tool for functional genomics and cancer biology research.
PANC-1 is a human pancreatic ductal adenocarcinoma cell line originally established from a primary tumor of the pancreas. It exhibits an epithelial morphology and retains key genetic features typical of pancreatic cancer, making it a widely utilized model for investigating tumor cell biology, including proliferation, invasion, and therapeutic resistance. This cell line is particularly valuable for dissecting signaling pathways that drive pancreatic cancer progression, and the TM4SF1 knockout derivative extends its utility for mechanistic studies focused on tetraspanin-mediated cellular processes.
TM4SF1 (Transmembrane 4 L Six Family Member 1) is a tetraspanin protein that functions as a molecular scaffold, facilitating the organization of protein complexes at the cell surface. It interacts with integrin ??1, integrin ??3, integrin ??6, CD44, and EGFR, and is activated by upstream regulators such as SP1, TGF-??, hypoxia, and EGF. Upon ligand engagement, TM4SF1 promotes integrin-mediated adhesion and signaling, leading to phosphorylation of FAK and Src, which in turn activate downstream effectors including ERK1/2 and AKT. This cascade enhances cell proliferation, migration, and survival, while also upregulating VEGF to stimulate tumor angiogenesis. TM4SF1 is implicated in multiple pathways, including integrin-mediated cell adhesion, FAK signaling, angiogenesis, and Wnt/??-catenin signaling, with representative components such as p130Cas, paxillin, VEGFR2, and eNOS contributing to its functional network.
In the context of pancreatic cancer, TM4SF1 is frequently overexpressed and correlates with aggressive disease characteristics. The TM4SF1 Knockout PANC-1 Cell Line therefore provides a physiologically relevant platform to dissect the contribution of TM4SF1 to pancreatic tumorigenesis. By comparing knockout and wild-type PANC-1 cells, researchers can elucidate how TM4SF1 modulates integrin-dependent signaling, cytoskeletal dynamics, and pro-angiogenic factor secretion. This model is instrumental for uncovering the mechanistic basis of TM4SF1-driven tumor progression and for evaluating the impact of its loss on key malignant phenotypes in a pancreatic ductal adenocarcinoma background.
This cell line supports a broad array of experimental applications, including functional studies of TM4SF1 in cell proliferation (MTT or BrdU assays), migration (Transwell or wound healing), invasion, and apoptosis. It can be employed in phospho-protein signaling arrays to map altered kinase activities, immunofluorescence to assess integrin localization, co-immunoprecipitation to probe TM4SF1-interacting complexes, and xenograft tumor growth assays to evaluate in vivo tumorigenicity. Additionally, it is suitable for drug resistance investigations and angiogenesis research, with validation via Western blotting, RT-qPCR, and Sanger sequencing of the CRISPR target site. For further technical information or to obtain this product, please contact Ascent Research.
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