The ACTA1 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of CAL-27 cells carrying targeted disruption of the ACTA1 gene. This model is generated by introducing loss-of-function mutations across the ACTA1 locus, yielding a heterogeneous pool of edited cells. As a polyclonal product, it does not originate from a single clone, providing a mixed population that reflects cellular diversity. It serves as a tool for studying ACTA1 function in a background of inherent variability.
CAL-27 is a human oral squamous cell carcinoma line derived from a tongue tumor, widely used as an in vitro model for head and neck cancer. These cells exhibit epithelial features and retain key malignant properties, including anchorage-independent growth and invasive potential. CAL-27 is genetically tractable and serves as a standard platform for investigating oncogenic signaling, drug responses, and cytoskeletal alterations in oral cancer.
ACTA1 encodes alpha-skeletal muscle actin, a filamentous actin isoform critical for contractile structures but also expressed in some non-muscle cells and tumors. Its expression is regulated by transcription factors such as SRF, MEF2, MyoD, YAP/TAZ, and TGF-beta signaling. ACTA1 interacts with actin-binding proteins including tropomyosin, cofilin, profilin, and alpha-actinin, and it participates in pathways with MYH, TNNI, and ACTN. Knockout of ACTA1 disrupts actin network integrity, altering cell adhesion, migration, and mechanotransduction, potentially through Hippo pathway modulation. These molecular interactions underscore ACTA1??s role in cytoskeletal dynamics and force transduction.
In CAL-27 cells, loss of ACTA1 disrupts actin filament organization, affecting focal adhesion turnover and cell motility. Since beta-actin predominates in non-muscle cells, this knockout enables isoform-specific dissection without global actin disruption. The polyclonal pool mimics tumor heterogeneity, allowing analysis of how mixed ACTA1-deficient and ACTA1-competent cells interact, compete, or adapt, thus providing insights into actin-dependent processes in oral squamous cell carcinoma progression.
This product supports studies of actin isoform functions in cancer, cytoskeletal remodeling, and drug sensitivity to actin-disrupting agents. Common assays include western blotting for ACTA1, phalloidin-based filament staining, migration/invasion assays, adhesion and proliferation measurements, and qPCR. It is also suitable for investigating actin-related muscle disease mechanisms in a non-muscle background. For additional details, contact Ascent Research.
