The KRT7 Knockout 143B Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the 143B human osteosarcoma cell line. The heterogeneous pool of edited cells enables targeted disruption of the KRT7 gene, creating a loss-of-function model for studying cytokeratin-7-dependent cytoskeletal dynamics, cell adhesion, and epithelial-mesenchymal transition (EMT) while avoiding clonal selection biases that can skew functional studies.
The 143B line originates from HOS/TE85 and harbors an activating KRAS mutation and p53 deficiency, representing a well-characterized mesenchymal tumor model. These osteoblast-like cells are widely employed in bone cancer research, metastasis studies, and signal transduction analyses due to their aggressive phenotype and genetic tractability for gene editing.
KRT7 encodes a type II intermediate filament protein that forms obligate heterodimers with KRT8 and KRT18, assembling into cytoskeletal networks essential for cellular architecture and mechanical stability. Its expression is transcriptionally regulated by SOX2, FOXA2, and NFKB1, and is responsive to TGFB1 and EGF. KRT7 interacts directly with KRT8, KRT18, KRT19, the chaperone HSPA8, and the adaptor YWHAZ. These filaments connect to focal adhesions via PTK2/FAK and to Rho GTPases, feeding into PI3K-AKT (AKT1) and MAPK (MAPK1) signaling to modulate adhesion and migration.
In the inherently mesenchymal 143B background, KRT7 knockout disrupts any residual intermediate filament networks, potentially reducing cell stiffness, adhesion strength, and directional motility. This system is particularly suited to investigate KRT7??s contribution to EMT plasticity, as partial or reverse transitions can occur in sarcomas during metastatic progression. Researchers can use this model to assess cytoskeletal remodeling and signaling crosstalk that drive invasive behavior.
This knockout cell product enables detailed phenotypic analyses using transwell migration and scratch wound assays for motility, immunofluorescence for intermediate filament architecture, and biophysical measurements of cell stiffness using atomic force microscopy. Quantitative RT-PCR panels targeting EMT markers (KRT8, KRT18, PTK2) and western blotting provide molecular validation. Applications extend to drug target validation, biomarker discovery, and mechanistic dissection of AKT1- and MAPK1-driven pathways in tumor cell biology. For additional product information, please contact Ascent Research.
