The APOBEC3C Knockout T-47D Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the T-47D human breast ductal carcinoma cell line, featuring targeted disruption of the APOBEC3C gene. This gene-edited product provides a loss-of-function model for studying the roles of APOBEC3C in innate immune and cancer-associated processes, without relying on single-cell clonal isolation. The polyclonal nature preserves population-level heterogeneity, making it suitable for assays where clonal uniformity is not required.
The host T-47D cell line originates from a pleural effusion of a breast ductal carcinoma and displays epithelial morphology with expression of estrogen receptor (ER), progesterone receptor (PR), and androgen receptor (AR). This ER-positive breast cancer model is widely employed in investigations of hormone-responsive signaling, endocrine therapy resistance, and tumor biology. Its well-characterized genetic background and reliable in vitro growth characteristics make it an appropriate platform for gene-editing approaches aimed at dissecting molecular mechanisms in luminal-type breast cancer.
APOBEC3C encodes a cytidine deaminase that mediates C-to-U editing of single-stranded DNA, playing dual roles in antiviral restriction and cancer mutagenesis. It is transcriptionally activated by type I and II interferons via JAK1/TYK2-mediated phosphorylation of STAT1 and STAT2, which complex with IRF9 to bind interferon-stimulated response elements. Additional upstream regulators include IRF1 and NF-??B. The enzyme targets retroviral cDNA and retrotransposon DNA, inhibiting replication, while its aberrant activity in tumor cells generates mutational signatures that drive heterogeneity. APOBEC3C physically interacts with HIV-1 Vif, other APOBEC3 members, and RNA-binding proteins in cytosolic granules.
In T-47D cells, an ER-positive breast cancer line, APOBEC3C knockout provides a tool to dissect its contributions to mutational processes and immune signaling within a hormonally responsive context. This model facilitates investigation of how loss of APOBEC3C impacts genomic stability, interferon-induced gene expression, and potential crosstalk between hormone signaling and innate immunity, relevant to APOBEC-driven mutagenesis in luminal breast cancers.
Researchers can employ this polyclonal knockout population in assays such as Western blotting and RT-qPCR for knockout validation, interferon stimulation experiments to assess canonical pathway activity, and DNA sequencing to detect APOBEC signature mutations. Viral restriction assays evaluate antiviral function, while cell proliferation and drug sensitivity assays explore cancer-relevant phenotypes. For additional information or technical assistance, please contact Ascent Research.
