The APOBEC3A Knockout T-47D Polyclonal Cells product consists of a polyclonal population of T-47D cells that have undergone CRISPR/Cas9-mediated disruption of the APOBEC3A gene, resulting in a loss-of-function model for the encoded cytidine deaminase. This polyclonal knockout format provides a heterogeneous cell pool carrying diverse editing events across the target locus, enabling robust functional studies without the clonal selection biases inherent to monoclonal knockouts. The genetically modified cell population is well suited for investigations into APOBEC3A-dependent processes in a human breast cancer background.
The host T-47D cell line originates from a pleural effusion metastasis of an invasive ductal breast carcinoma and is widely used as an in vitro model of estrogen receptor-positive (ER+), progesterone receptor-positive (PR+), and androgen receptor-expressing luminal breast cancer. These cells retain luminal epithelial features and hormone responsiveness, making them particularly valuable for studying hormone-dependent breast cancer biology, therapeutic responses, and endocrine resistance mechanisms.
APOBEC3A belongs to the APOBEC family of cytidine deaminases that catalyze the conversion of cytosine to uracil in single-stranded DNA. Its enzymatic activity is upregulated by type I and type II interferons (IFN-??, IFN-??, IFN-??) and NF-??B, linking it to innate antiviral immunity. In the nucleus, APOBEC3A interacts with PCNA and RPA on single-stranded DNA substrates, and its deamination products are processed by base excision repair components such as uracil DNA glycosylase (UNG) and AP endonuclease, as well as mismatch repair proteins and translesion synthesis polymerases. While this activity restricts viral replication by editing viral DNA, it also introduces C-to-T transitions and DNA strand breaks in the host genome, contributing prominently to the mutational landscapes of breast cancers and other APOBEC-associated malignancies.
In the T-47D background, which is inherently ER+ and PR+, APOBEC3A knockout allows direct interrogation of the deaminase’s role in driving somatic mutagenesis and genomic instability in hormone-responsive breast cancer. Given the high frequency of APOBEC mutation signatures in breast cancer genomes, this polyclonal knockout model provides a valuable tool to dissect the contribution of APOBEC3A to cancer evolution, therapy resistance, and the interplay between hormonal signaling and innate immune pathways.
The APOBEC3A Knockout T-47D Polyclonal Cells are suited for a range of applications, including examining the role of APOBEC3A-mediated mutagenesis in breast cancer progression via whole-genome sequencing to identify mutation signatures, assessing interferon-induced antiviral responses through RT-qPCR and western blotting, and evaluating drug sensitivity under various therapeutic regimens. Functional cytidine deamination activity can be monitored by differential DNA denaturation PCR (3D-PCR), and the impact on DNA repair pathways can be studied using comet assays or immunofluorescence for DNA damage markers. These cells also enable investigation of how APOBEC3A contributes to acquired drug resistance, providing a platform for screening combination therapies that target DNA repair vulnerabilities. For additional details and support, please contact Ascent Research.
