The CADM1 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population engineered to disrupt the CADM1 gene in the human near-haploid HAP1 cell line. This heterogeneous pool of gene-edited cells provides a powerful loss-of-function model for studying CADM1-dependent processes without requiring single-cell cloning. The targeted gene disruption impairs CADM1-mediated functions, enabling investigation of its role in cell adhesion and tumor suppression.
The HAP1 cell line is a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia line. With a stable haploid karyotype, HAP1 cells are widely adopted for genetic knockout studies due to the simplified genotype that eliminates functional redundancy from a second allele. This characteristic makes HAP1 an ideal host for exploring the phenotypic consequences of single-gene disruptions, particularly for genes involved in complex signaling networks and tumorigenesis.
CADM1 (Cell Adhesion Molecule 1), also known as TSLC1, is a Ca2?-independent homophilic and heterophilic cell adhesion molecule that maintains epithelial integrity and contact inhibition. Its expression is regulated by the SP1 transcription factor and modulated by ADAM10/17-mediated ectodomain shedding and TGF-?? signaling. CADM1 interacts with Nectin-3 and DAL-1/protein 4.1B to link to the actin cytoskeleton, and its tumor-suppressive functions are mediated through downstream effectors such as the cell cycle inhibitors p21 and p27, pro-apoptotic caspases-3 and -9, and tight junction proteins like claudins. Loss of CADM1 disrupts these pathways, enabling activation of PI3K/Akt (involving Akt1 and PTEN) and Hippo pathway effectors YAP1/TAZ, which drive proliferation and epithelial-mesenchymal transition.
In the near-haploid HAP1 background, CADM1 knockout provides a simplified genetic system to study its tumor-suppressive roles. The lack of a second allele increases phenotypic clarity, allowing robust analysis of cell adhesion, migration, invasion, and apoptosis. This model is especially relevant for cancers with frequent CADM1 downregulation, including non-small cell lung, breast, cervical, and hepatocellular carcinomas, as well as for investigating its link to autism spectrum disorder.
These knockout cells support diverse applications: cell adhesion and migration assays, proliferation and apoptosis studies, co-immunoprecipitation, and high-throughput drug screening. Standard techniques such as Western blotting, RT-qPCR, immunofluorescence, and flow cytometry validate target disruption and pathway alterations, while RNA-seq and xenograft models enable comprehensive mechanistic and preclinical investigations. For details, pricing, or technical support, please contact Ascent Research.
