The ACTC1 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of CAL-27 cells with targeted disruptions in the ACTC1 gene. This heterogeneous pool enables loss-of-function studies of cardiac alpha-actin in a human cancer background, avoiding clonal selection artifacts. The polyclonal format retains genetic diversity while achieving gene disruption across the population, providing a robust model for investigating actin isoform-specific functions.
The CAL-27 cell line is derived from a tongue squamous cell carcinoma of a 56-year-old male and exhibits adherent epithelial morphology. It is a well-established model for oral squamous cell carcinoma, characterized by dysregulated proliferation, migration, and invasion. CAL-27 cells offer a reproducible system for studying cancer progression and cytoskeletal dynamics.
ACTC1 encodes cardiac alpha-actin, a major component of the sarcomeric thin filament essential for cardiac muscle contraction. Its transcription is regulated by SRF, myocardin, and MEF2C downstream of TGF-beta, and the protein interacts with myosin, tropomyosin, troponin, alpha-actinin, and nebulin. Downstream targets include myosin heavy chains, tropomyosins, and troponins. In cardiomyocytes, ACTC1 coordinates with MYH6, TNNT2, TPM1, and MYBPC3 to generate force. In non-muscle cells, ectopic ACTC1 expression or actin isoform switching can alter cytoskeletal organization and motility, making this knockout a tool for dissecting actin-dependent processes in cancer.
ACTC1 disruption in CAL-27 allows researchers to probe the role of cardiac alpha-actin in cancer cell motility and cytoskeletal remodeling, even in the absence of sarcomeres. This model is valuable for studying actin isoform compensation, migration-related signaling, and actinopathy mechanisms in a tumorigenic context. The polyclonal knockout population also captures heterogeneous cellular responses, reflecting the complexity of solid tumors.
Applications include confirming knockout by western blotting and RT-qPCR, assessing actin localization with immunofluorescence, and measuring effects on migration and proliferation using wound-healing and growth assays. The cells are suitable for rescue studies with exogenous ACTC1 variants to dissect structure-function relationships. For additional information, please contact Ascent Research.
