The ANLN Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human colorectal carcinoma HCT 116 cell line, engineered to disrupt ANLN gene expression and generate a loss-of-function model for advanced biomedical research. This polyclonal population provides a heterogeneous pool of knockout cells, enabling robust study of ANLN-dependent processes without clonal selection artifacts.
The host HCT 116 cell line is a well-characterized human colon carcinoma model originating from an adult male, featuring KRAS G13D and PIK3CA mutations, microsatellite stability (MSS), and mismatch repair proficiency. This genetic background renders HCT 116 cells particularly valuable for investigating colorectal cancer biology, intracellular signaling pathways, and pharmacological responses, offering a clinically relevant context for gene disruption studies.
ANLN encodes anillin, a multidomain actin-binding scaffold protein that orchestrates cytokinesis by recruiting and organizing key contractile ring components. Anillin interacts directly with F-actin, myosin II, and septins (SEPT2, SEPT6, SEPT7) and is regulated by RhoA GTPase, cyclin-dependent kinase CDK1, and the anaphase-promoting complex/cyclosome (APC/C). It functions downstream of E2F transcription factors and is integrated into the PI3K/AKT/mTOR pathway, cooperating with RhoA effectors like Ect2 and CYK-4 to ensure cleavage furrow ingression and abscission. Additionally, anillin stabilizes E-cadherin-mediated cell?Ccell junctions, linking cytokinesis with cell migration and epithelial integrity.
In the HCT 116 background, ANLN disruption is anticipated to impair cytokinesis completion, leading to multinucleation, polyploidy, and genomic instability. The coexistence of oncogenic KRAS and PIK3CA mutations may exacerbate these cytokinetic defects, influencing tumorigenic phenotypes and drug sensitivity. Furthermore, loss of ANLN is expected to compromise actomyosin contractility and cell?Ccell junction maintenance, altering migratory and invasive properties. This model thus provides a powerful tool to dissect the intersection of cytokinetic failure, oncogenic signaling, and epithelial malignancy in colorectal carcinoma.
Applications include detailed functional studies of ANLN in cytokinesis and cell cycle progression, investigations of cancer cell migration and invasion using Transwell assays, time-lapse microscopy to monitor mitotic abnormalities, flow cytometric analysis of DNA content for polyploidy assessment, and phalloidin staining for cytoskeletal organization. The polyclonal knockout cells are also suitable for synthetic lethality screens targeting KRAS or PIK3CA mutant cancers, drug response profiling, and global transcriptomic analyses via RNA-seq. For additional product information and technical support, please contact Ascent Research.
