The ANLN Knockout T-47D Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the human T-47D breast epithelial cell line, with targeted disruption of the endogenous ANLN gene. This polyclonal knockout product circumvents clonal artifacts, providing a genetically diverse loss-of-function model for anillin studies. CRISPR/Cas9-mediated gene editing abrogates anillin’s scaffolding function, enabling dissection of its roles in cytokinesis, actomyosin organization, and genomic integrity. This model system is suitable for cancer biology and drug discovery applications.
T-47D is a human breast ductal carcinoma cell line derived from pleural effusion, widely used as a luminal A, hormone-responsive model. It expresses estrogen receptor (ER), progesterone receptor (PR), and androgen receptor (AR), retaining hormone-dependent growth and a well-differentiated phenotype. This line recapitulates key features of luminal breast tumors, including active ER signaling, making it ideal for studying endocrine therapy mechanisms. Incorporating ANLN knockout into this context permits investigation of anillin’s impact on hormone-responsive breast cancer progression and genomic instability.
ANLN encodes anillin, a conserved actin-binding scaffold that coordinates contractile ring assembly at the cleavage furrow during cytokinesis. Anillin directly binds RhoA, F-actin, and myosin II, facilitating furrow ingression and daughter cell separation. Functioning downstream of RhoA, anillin integrates with cytokinesis regulators including Ect2, RacGAP1, and Citron kinase, while its transcription is driven by E2F1, FOXM1, and MYC. The anillin-RhoA axis operates within a broader network comprising ROCK, mDia, and Profilin to modulate actin dynamics. Consequently, ANLN disruption dismantles this structural and signaling hub, leading to failed cytokinesis, multinucleation, and genomic instability.
In luminal A T-47D breast cancer cells, ANLN loss-of-function is especially significant given anillin’s overexpression in tumors and association with poor prognosis. ANLN knockout induces multinucleation and chromosomal instability, fueling tumor heterogeneity in hormone-responsive backgrounds. This model enables examination of anillin deficiency effects on ER/PR signaling, cell cycle progression, and endocrine resistance. It also facilitates study of anillin’s interplay with RhoA pathways that control actomyosin contractility, migration, and invasion. Thus, it provides a physiologically relevant system to dissect anillin’s contributions to genomic instability and metastasis in luminal breast cancers.
These knockout cells are suited for cytokinesis assays??immunofluorescence microscopy of contractile ring components, multinucleation scoring, and time-lapse imaging of mitotic failure. Cell cycle analysis by flow cytometry, proliferation assays, and Western blotting for mitotic regulators (e.g., cyclins, phospho-histone H3) delineate anillin loss effects. Migration, invasion, and drug sensitivity testing against chemotherapeutics or targeted agents evaluate anillin??s roles in motility and therapeutic response. RT-qPCR and transcriptomic profiling can uncover transcriptional changes in E2F1, FOXM1, and MYC target genes. For additional specifications, customization options, or collaborative inquiries, please contact Ascent Research.
