The ANLN Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population in which the ANLN gene has been disrupted via CRISPR/Cas9-mediated gene editing. This product is supplied as a heterogeneous polyclonal population, ensuring representation of diverse editing events without single-cell cloning. The ANLN gene encodes anillin, an actin-binding scaffold protein critical for cytokinesis and actomyosin contractile ring assembly. By ablating ANLN expression in this polyclonal pool, researchers can study loss-of-function effects in a population context, avoiding clonal selection bias and enabling robust functional genomics analyses.
The parental Ca Ski cell line is a widely used model of human cervical epidermoid carcinoma, originally derived from a small intestine metastasis. These cells are HPV16-positive and retain integrated human papillomavirus type 16 sequences, which drive constitutive expression of the viral oncoproteins E6 and E7. This genetic background disrupts p53 and retinoblastoma tumor suppressor pathways, promoting uncontrolled proliferation and genomic instability. Ca Ski cells are emblematic of HPV-driven cervical carcinogenesis and serve as a relevant platform for exploring oncogenic signaling, metastasis, and therapeutic intervention.
Anillin is a multidomain scaffold coordinating actomyosin contractility during cytokinesis and migration. It directly binds F-actin, myosin II, and septins (SEPT2, SEPT6, SEPT7), and is recruited to the cleavage furrow by the RhoA GEF ECT2 and citron kinase. ANLN transcription is controlled by E2F factors and responsive to RhoA, PI3K/AKT, and MAPK signaling; in Ca Ski cells, it is additionally modulated by HPV16 E6/E7, linking viral oncogenesis to cytoskeletal dynamics. Disruption of ANLN ablates anillin-dependent signaling, impairing actomyosin ring and septin assembly.
In HPV16-positive cervical carcinoma, ANLN knockout provides a powerful model to dissect the intersection between viral oncogenes and host cell division machinery. Loss of anillin leads to cytokinesis failure, resulting in multinucleation, aneuploidy, and altered cell migration and invasion ?C traits associated with tumor progression. By eliminating anillin in Ca Ski cells, researchers can explore how HPV-driven pathways rely on cytoskeletal regulators to maintain malignant phenotypes, potentially revealing vulnerabilities for therapeutic exploitation, such as combination strategies targeting the cell cycle or Rho GTPase signaling.
This polyclonal knockout cell population is suitable for a range of experimental approaches, including Western blotting and RT-qPCR for target confirmation, immunofluorescence for anillin and contractile ring components, flow cytometry for DNA content/polyploidy, wound healing and Matrigel invasion assays, and co-immunoprecipitation or live-cell imaging. Typical research applications include studying cytokinesis dysfunction in cancer, modeling HPV-driven cervical carcinoma progression, and validating drug targets that impinge on actin cytoskeletal regulation. For additional information or custom inquiries, please contact Ascent Research.
