The ANLN Knockout 143B Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal human cell population in which the ANLN gene has been disrupted. This loss-of-function model is generated in the 143B osteosarcoma cell line and is supplied as a polyclonal knockout pool suitable for functional genomics, pathway dissection, and anticancer studies. The polyclonal format avoids clonal selection artifacts, enabling more representative assessment of ANLN-dependent phenotypes across a heterogeneous genetic background.
The 143B cell line is a well-characterized human osteosarcoma model with epithelial morphology and demonstrated tumorigenicity. Derived from a bone cancer specimen, these cells serve as a robust platform for studying malignant osteoblast biology, metastasis, and therapeutic responses. The tumorigenic nature of 143B cells makes them particularly relevant for investigating genes that regulate proliferation and cytokinesis in the context of bone cancer.
ANLN encodes anillin, an actin-binding scaffolding protein essential for organizing the cleavage furrow during cytokinesis. Anillin directly binds F-actin, myosin II, and septins (septin2,6,7), and interacts with Rho pathway effectors ECT2 and RacGAP1. It is regulated by E2F1 transcription, RhoA GTPase, and Aurora B kinase, which control its localization and activity. Anillin scaffolds the actomyosin ring and septin filaments, coordinating RhoA?CROCK?Ccitron kinase signaling and myosin light chain phosphorylation to ensure mitotic exit and daughter cell separation.
Disruption of ANLN in 143B cells leads to cytokinesis failure, multinucleation, polyploidy, and genomic instability??phenotypes highly relevant to osteosarcoma, which often exhibits complex karyotypes. As ANLN is overexpressed in multiple cancers, this knockout model facilitates dissection of its role in tumor cell division and proliferation. Using the 143B background, researchers can investigate how ANLN loss affects bone cancer cell behavior, including proliferation, colony formation, and response to anti-mitotic agents.
Typical applications include live-cell imaging of cytokinesis failure, immunofluorescence microscopy of actin and tubulin, flow cytometry for DNA content and multinucleation, and western blotting for ANLN or phospho-MLC. Proliferation (MTT, IncuCyte), colony formation, and RhoA activation assays enable detailed functional profiling. The knockout model supports anti-mitotic drug screening, polyploidy studies, and osteosarcoma progression modeling. For further details, contact Ascent Research.
