The KRT14 Knockout DLD-1 Polyclonal Cells represent a heterogeneous CRISPR/Cas9-edited polyclonal knockout population derived from the DLD-1 human colorectal adenocarcinoma cell line, designed to disrupt the KRT14 gene. This product provides a pool of cells carrying targeted gene disruptions, enabling robust loss-of-function analyses without the genetic bottlenecks inherent to clonal selection. By abolishing keratin 14 (KRT14) expression, the cells serve as a versatile platform for investigating intermediate filament biology and its interplay with oncogenic signaling in an epithelial context.
The DLD-1 cell line, originating from a colorectal adenocarcinoma, is a well-established model of intestinal epithelial biology and colorectal cancer. Widely utilized in cancer research and drug screening, DLD-1 cells retain key characteristics of epithelial polarity and signal transduction pathways, including active WNT, EGFR, and Notch cascades. This background is particularly suited for dissecting the contributions of structural proteins to tumor cell behavior, given the cell line??s tractability for genetic manipulation and common use in migration, invasion, and adhesion studies.
KRT14 encodes a type I keratin that obligately pairs with KRT5 to form intermediate filament heterodimers, which are transcriptionally controlled by TP63 downstream of EGFR and WNT signaling. KRT14 filaments provide mechanical resilience to epithelial cells by anchoring to desmosomes and hemidesmosomes through interactions with desmoplakin, plakins, and 14-3-3 proteins. Beyond its structural role, KRT14 influences AKT signaling, thereby integrating physical scaffold functions with growth factor responses. Disruption of KRT14 in DLD-1 cells eliminates this filament network, abrogating TP63-mediated keratinization programs and potentially uncoupling EGFR/ERK signaling from cytoskeletal organization, which collectively perturbs cell adhesion, polarity, and migratory capacity.
In the colorectal adenocarcinoma context, KRT14 expression is often associated with aggressive subtypes and epithelial-mesenchymal transition, making its knockout in DLD-1 cells a powerful tool to probe keratin-dependent mechanisms of tumor progression. By removing KRT14, researchers can delineate how intermediate filament disruption affects signaling through EGFR, Notch, and AKT, and evaluate consequent changes in cell adhesion, migration, and invasion. This model is invaluable for deciphering the molecular basis of cancer cell plasticity and for testing whether KRT14 loss sensitizes cells to targeted therapies or chemotherapeutic agents.
These polyclonal knockout cells are suitable for a range of functional and molecular assays, including western blotting, immunofluorescence, RT-qPCR, and cell-based assays for migration, invasion, and adhesion. They facilitate detailed studies of keratin function in colorectal cancer, epithelial-mesenchymal transition, intermediate filament dynamics, and drug response modulation. For technical inquiries and ordering information, please contact Ascent Research.
