The ANLN Knockout LoVo Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ANLN gene in the human LoVo colorectal adenocarcinoma cell line. This polyclonal knockout model is generated through CRISPR/Cas9-mediated gene disruption, resulting in a mixed population of cells harboring loss-of-function modifications at the ANLN locus. As a polyclonal pool, it captures the diversity of editing outcomes and provides a robust system for studying ANLN function without the selection bias of single-cell-derived clones.
The parental LoVo cell line derives from a lymph node metastasis of a human colorectal adenocarcinoma and serves as a well-established model for metastatic colorectal cancer. These epithelial cells exhibit characteristic features of aggressive colorectal carcinoma and are widely employed in cancer research to investigate tumor cell proliferation, migration, and drug response. The LoVo background provides a clinically relevant context for examining the role of ANLN in colorectal cancer progression.
ANLN encodes anillin, a conserved actin-binding protein that scaffolds the contractile ring during cytokinesis, connecting the plasma membrane to the actomyosin network. Anillin interacts with key cytoskeletal components including actin, myosin, and septins, as well as mitotic regulators ECT2 and RACGAP1. Its expression is transcriptionally regulated by E2F1 and FOXM1, and it operates downstream of the RhoA signaling cascade. RhoA activates ROCK and Citron kinase, which phosphorylate myosin light chain to drive contractile ring constriction. ANLN organizes these effectors to ensure proper furrow ingression and abscission. Consequently, disruption of ANLN in LoVo cells leads to cytokinesis failure, yielding multinucleated cells and a marked reduction in proliferation.
In colorectal cancer, ANLN is frequently upregulated and associated with advanced tumor stage and poor prognosis. The ANLN knockout in the LoVo metastatic colorectal adenocarcinoma model therefore allows researchers to dissect the functional role of anillin in cancer cell division and tumor aggressiveness. Loss of ANLN impairs the ability of these cells to complete cytokinesis, providing a unique platform to study multinucleation-induced genomic instability and to evaluate therapeutic strategies targeting mitotic exit. This model is particularly relevant for exploring RhoA pathway dependencies and for identifying vulnerabilities in ANLN-deficient cancer cells.
Typical research applications for the ANLN Knockout LoVo Polyclonal Cells include cancer cell division studies, cytokinesis failure analysis, and anti-mitotic drug testing. Investigators can employ immunofluorescence microscopy to visualize the contractile ring components (such as myosin II and septins) or to quantify multinucleation frequencies. Flow cytometry permits detailed cell cycle profiling and assessment of polyploidy, while proliferation, migration, and invasion assays enable functional characterization of ANLN loss in a metastatic colorectal cancer context. These polyclonal knockout cells thus support a broad range of experimental workflows for both basic and translational research. For further technical specifications and ordering details, please contact Ascent Research.
