The KRT14 Knockout CAL-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the KRT14 gene has been disrupted in the CAL-27 human oral squamous cell carcinoma line. This heterogeneous pool of gene-edited cells avoids clonal selection artifacts, enabling functional interrogation of KRT14 at the population level while retaining the inherent genetic diversity of the tumor cell line. The polyclonal nature ensures that phenotypes reflect the average behavior of a genetically diverse population, mirroring native tumor heterogeneity. The CRISPR/Cas9-mediated gene disruption provides a robust loss-of-function model for analyzing KRT14-dependent processes in critical epithelial cancer biology.
The parental CAL-27 cell line, established from a tongue squamous cell carcinoma of a 56-year-old male patient, is a widely utilized model for oral squamous cell carcinoma (OSCC). These adherent epithelial cells exhibit basal keratin expression, retain desmosomal and hemidesmosomal structures, and are capable of forming tumors in immunocompromised mice, thus offering a faithful context for investigating keratin-associated tumor processes.
KRT14 encodes a type I intermediate filament protein that obligately assembles with KRT5 into the cytoskeletal network of basal epithelial cells, critical for mechanical integrity, adhesion, and migration. Transcription is driven by TP63 and modulated by AP-1 factors (FOS, JUN) and ??-catenin (CTNNB1) downstream of EGF and TGFB1. KRT14 interacts with DSP, PLEC, and JUP to tether filaments to desmosomes and hemidesmosomes, and it regulates ITGB4 and actin remodeling, impacting PI3K-AKT signaling.
In CAL-27 OSCC cells, KRT14 disruption destabilizes KRT5/KRT14 filaments, impairing cell cohesion and attenuating EMT-associated invasiveness (involving SNAI1 and CDH1). Hemidesmosome weakening may suppress integrin-PI3K-AKT survival signaling, altering responses to mechanical and therapeutic stress. Thus, this polyclonal knockout model enables detailed dissection of keratin network roles in tumor cell plasticity and mechanosensitivity.
This polyclonal knockout model is suited for investigating KRT14’s role in OSCC invasion and metastasis using transwell migration/invasion assays, wound healing, and immunofluorescence to visualize keratin network disruption. Other applications include transcriptomic profiling via RNA-seq, drug sensitivity testing (e.g., cisplatin), apoptosis analysis, co-immunoprecipitation with KRT5, and cell adhesion assays. For additional technical information, please contact Ascent Research.
