The ACTC1 Knockout DLD-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from DLD-1 cells, engineered to disrupt the ACTC1 gene. This heterogeneous knockout model allows loss-of-function studies of alpha-cardiac actin in an epithelial cancer background. The polyclonal format provides a versatile tool for functional screening, capturing diverse gene-editing events without clonal selection.
DLD-1 is a human colorectal adenocarcinoma cell line with oncogenic mutations in APC, KRAS, and TP53, representing a model of colorectal tumorigenesis with dysregulated Wnt signaling, KRAS-driven proliferation, and compromised p53. These epithelial cells exhibit robust adherent growth and invasive capacity, offering a suitable host for studying actin cytoskeletal dynamics in colorectal cancer.
ACTC1 encodes alpha-cardiac actin, a highly conserved actin isoform that polymerizes into thin filaments within sarcomeres of cardiac muscle and contributes to the actin cytoskeleton in non-muscle cells. In cardiac tissue, ACTC1 is transcriptionally activated by SRF, myocardin, GATA4, MEF2, and NKX2-5, and is modulated by TGF-beta and Wnt signaling. The protein interacts with myosin heavy chain, tropomyosin, troponin, and alpha-actinin to form contractile units, while filament dynamics involve cofilin and profilin. Downstream, ACTC1 organizes actin filaments that scaffold myosin motors and cell adhesion complexes. It functions within a network that includes MYH6, TPM1, TNNT2, TNNI3, TNNC1, ACTN2, and NEXN, governing striated muscle contraction and actin cytoskeletal organization.
In the DLD-1 colorectal adenocarcinoma model, ACTC1 knockout is expected to disrupt actin cytoskeletal organization, potentially impairing cell morphology, migration, invasion, and adhesion??processes frequently hijacked in cancer metastasis. Although primarily studied in cardiac muscle, alpha-cardiac actin is also expressed in certain non-muscle contexts, and its ablation in DLD-1 cells provides a unique platform to delineate isoform-specific functions of actin in oncogenic signaling and cytoskeletal mechanics. This loss-of-function model may reveal compensatory roles of other actin isoforms and uncover vulnerabilities linked to actin-dependent processes in colorectal cancer cells harboring APC, KRAS, and TP53 mutations.
Researchers can employ this knockout cell population for functional dissection of actin cytoskeleton-mediated events in colorectal cancer, including quantitative live-cell imaging of F-actin dynamics via phalloidin staining, transwell migration and invasion assays, and co-immunoprecipitation of actin-binding partners such as alpha-actinin or tropomyosin. The model is suited for drug target validation studies focused on cardiomyopathies, where ACTC1 mutations are linked to hypertrophic and dilated cardiomyopathies, atrial septal defects, and congenital heart defects. Transcriptomic profiling by RNA-seq and protein expression analysis by Western blotting and RT-qPCR can be used to characterize the molecular consequences of ACTC1 loss, while immunofluorescence enables spatial assessment of cytoskeletal reorganization. These applications support a broad range of investigations from basic actin biology to translational oncology and cardiovascular disease research. For further inquiries or technical assistance, please contact Ascent Research.
