The KRT18 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human tongue squamous cell carcinoma line CAL-27, carrying a targeted disruption of the KRT18 gene. This model provides a heterogenous knockout pool that minimizes clonal artifacts while enabling loss-of-function studies of type I cytokeratin 18. Suitable for investigating epithelial cell integrity and cancer biology, the polyclonal format reflects natural cancer cell heterogeneity and is ideal for functional assays such as migration, apoptosis, and drug response.
The CAL-27 cell line was established from a tongue squamous cell carcinoma of a 56-year-old male patient. It is a widely employed model in head and neck cancer research, retaining key epithelial traits including cytokeratin expression. CAL-27 provides a pathophysiologically relevant background for examining KRT18 function, as its intermediate filament network is integral to the malignant phenotype and therapeutic response of oral squamous cell carcinoma.
KRT18 is a type I cytokeratin that forms obligate heterodimers with its type II partner KRT8, assembling intermediate filament networks that confer mechanical resilience to epithelial cells. Beyond structural roles, KRT18 participates in signaling: it is transcriptionally regulated by AP-1, Sp1, p53, TGF-beta, and TNF-alpha. During apoptosis, Caspase-3-mediated cleavage produces fragments that interact with TRADD and 14-3-3 proteins, modulating downstream effectors such as AKT1 and Bcl-2. KRT18 also associates with desmoplakin, annexin A2, and HSP70 at desmosomes and stress response sites. Knockdown of KRT18 disrupts keratin filaments and promotes epithelial-mesenchymal transition (EMT), with associated changes in E-cadherin and PI3K/AKT pathway activity, placing it at a nexus of structural integrity and signaling.
In CAL-27 cells, KRT18 knockout provides a clinically relevant system to dissect the contribution of intermediate filaments to cancer hallmarks. Loss of KRT18 disrupts cytoskeletal organization, alters cell adhesion, and sensitizes cells to extrinsic stresses, making this model valuable for studying head and neck cancer invasion and EMT. The polyclonal knockout avoids clonal selection bias, enabling assessment of population-level heterogeneity in drug sensitivity, migratory capacity, and apoptotic priming. This model thus offers a robust platform for translational oncology research in a background that mirrors the genetic context of oral squamous cell carcinoma.
These polyclonal knockout cells are suited for a range of assays: western blotting and immunofluorescence to monitor KRT18 and EMT marker expression; wound healing and Transwell invasion assays to quantify cell motility; Annexin V/PI staining for apoptosis; RT-qPCR profiling of EMT-related genes; and drug sensitivity screens using cisplatin or cetuximab. Together, these approaches enable comprehensive functional analysis of KRT18 in cancer progression. For further technical details or custom requests, please contact Ascent Research.
