The KRT18 Knockout DLD-1 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout population in which the KRT18 gene has been disrupted. This product provides a heterogeneous loss-of-function model in the DLD-1 human colorectal adenocarcinoma cell line. The polyclonal format captures a variety of CRISPR/Cas9-mediated gene disruptions without single-cell cloning, minimizing clonal bias and offering a physiologically relevant system for functional studies.
The DLD-1 host cell line is a well-characterized human colorectal adenocarcinoma epithelial cell line derived from a male patient. These cells exhibit an epithelial morphology, are tumorigenic, and maintain key features of colon epithelium, making them a robust model for colorectal carcinoma research. DLD-1 cells are extensively used to investigate mechanisms of colon cancer progression, metastasis, drug resistance, and epithelial homeostasis.
Keratin 18 is a type I intermediate filament protein that heterodimerizes with keratin 8 (KRT8) to form the cytoskeletal network in simple epithelia, providing mechanical support and structural integrity. It also participates in signal transduction: KRT18 is regulated by kinases such as Akt and PKC, and transcriptionally controlled by p53, AP-1, and Sp1. Upon apoptosis, it is cleaved by caspase-3 and -6; the resulting fragments bind 14-3-3 proteins and modulate pro-survival signaling. KRT18 further interacts with TRADD and Fas-associated death domain, linking it to death receptor pathways. Thus, KRT18 serves as a mechanosensitive signaling scaffold that integrates stress and survival cues.
Disruption of KRT18 in DLD-1 cells compromises the keratin intermediate filament network, likely altering mechanical stability and apoptosis sensitivity. Loss of KRT18 disrupts heterodimerization with KRT8 and may reduce pro-survival signaling through 14-3-3 and the PI3K/Akt and MAPK pathways. Given KRT18’s role in EMT and TGF-?? signaling, this model enables dissection of how keratin dynamics influence colorectal cancer cell plasticity, migration, and invasion.
This knockout model is suitable for Western blotting (KRT18, cleaved caspase-3), immunofluorescence for intermediate filaments, apoptosis assays (Annexin V/PI, caspase activity), drug sensitivity screens (MTT, colony formation), migration/invasion assays, and co-immunoprecipitation with KRT8 or 14-3-3. It facilitates studies of keratin 18 in colorectal cancer pathogenesis, apoptosis regulation, EMT, and therapeutic resistance. For further details, contact Ascent Research.
