ACTR1B Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human CAL-27 epithelial cell line. This loss-of-function model targets the ACTR1B gene, which encodes a core dynactin complex subunit. The polyclonal format provides a heterogeneous cell pool, facilitating broad functional investigations of ACTR1B-dependent processes without clonal selection artifacts.
The parental CAL-27 line is a well-characterized epithelial cell model originating from a human tongue squamous cell carcinoma. These cells are HPV-negative and harbor a mutant p53 tumor suppressor, reflecting a commonly encountered genetic profile in head and neck cancers. CAL-27 cells are widely employed for studying oncogenic signaling, invasion, and drug response, making this knockout system particularly relevant for cancer-focused cytoskeletal research.
ACTR1B is an integral constituent of the dynactin complex, functioning as a critical cofactor for cytoplasmic dynein. It directly interacts with key dynactin components, including DCTN1/p150Glued, DCTN2/p50, and ACTR1A, as well as the dynein heavy chain DYNC1H1 and intermediate chains DYNC1I1/2. This network orchestrates dynein-dependent retrograde transport along microtubules, facilitating mitotic spindle assembly, vesicle trafficking, and autophagosome transport. ACTR1B expression is regulated by cell cycle-dependent transcription factors such as E2F, repressed by p53, and modulated by post-translational modifications like acetylation and phosphorylation. Downstream, dynactin-dynein activity controls adaptor proteins BICD2 and HOOK3, mitotic checkpoint proteins, and endosomal/lysosomal trafficking machinery, thus integrating ACTR1B into essential cellular pathways.
Given the importance of proper mitotic progression and intracellular transport in cancer cell proliferation, ACTR1B disruption in CAL-27 cells provides a powerful system to study tumorigenic mechanisms. The p53-mutant background relieves transcriptional repression of ACTR1B, potentially exacerbating mitotic susceptibility. Head and neck squamous cell carcinomas frequently exhibit chromosomal instability and trafficking defects, phenotypes tied to dynactin function. This knockout model is therefore well-suited for investigating spindle organization errors, cargo mislocalization, and their contributions to tumor cell proliferation and motility.
Researchers can employ this product for diverse experimental approaches, including Western blotting, RT-qPCR, immunofluorescence, and flow cytometry for cell cycle analysis. Functional assays such as mitotic index scoring, live-cell imaging of dynein-dependent cargo transport, and co-immunoprecipitation with DCTN1 or BICD2 are readily performed. Drug screening for cytoskeletal or autophagy inhibitors, as well as migration and invasion assays, can dissect ACTR1B roles in cancer cell behavior. For further details or technical support, please contact Ascent Research.
