Description

The Brd7 Knockout 4T07 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the murine 4T07 mammary carcinoma line, designed for targeted disruption of the Brd7 gene. This loss-of-function model enables stable ablation of Brd7 expression, providing a reliable tool for studying the tumor-suppressive roles of Brd7 in a syngeneic BALB/c mammary tumor background.

The parental 4T07 cell line was established from a spontaneous BALB/c mouse mammary carcinoma and is extensively utilized as a syngeneic model for breast cancer. These cells form tumors efficiently when implanted into immunocompetent BALB/c mice, providing a microenvironment that closely mirrors human disease. The 4T07 model is particularly valued for studying tumor suppressor gene functions, metastasis-associated mechanisms, and for evaluating novel therapies in vivo.

Brd7 is a critical subunit of the PBAF subclass of SWI/SNF ATP-dependent chromatin remodeling complexes. It functions as a tumor suppressor by directly binding and stabilizing the p53 transcription factor, thereby potentiating p53-mediated transcriptional activation. This interaction upregulates key downstream effectors including the cyclin-dependent kinase inhibitor p21 (Cdkn1a), the pro-apoptotic Bcl-2 family members Bax and PUMA (Bbc3), which collectively induce cell cycle arrest and apoptosis. Brd7 also forms complexes with other SWI/SNF components such as BRG1 (SMARCA4) and BAF180 (PBRM1). Upstream, Brd7 activity is modulated by DNA damage signaling pathways that activate p53, positioning Brd7 as a vital bridge between chromatin dynamics and tumor suppressive gene expression programs.

In the 4T07 mammary carcinoma background, deletion of Brd7 offers a robust system to investigate the tumor-suppressive role of this chromatin remodeler. Loss of Brd7 is predicted to dampen p53 transcriptional output, impairing the expression of p21, Bax, and PUMA, thereby reducing cell cycle arrest and apoptotic responses. This cell line thus enables exploration of how Brd7 deficiency drives proliferation and survival, and can be used to assess sensitivity to DNA-damaging chemotherapeutics that rely on wild-type p53 activity. Comparisons with parental 4T07 cells clarify Brd7-dependent phenotypes in tumorigenesis.

Researchers can apply the Brd7 Knockout 4T07 Cell Line to a range of experimental workflows, including breast cancer progression studies, p53 signaling dissection, and chromatin remodeling analyses. Practical assays include western blotting and RT-qPCR for gene and protein expression profiling, MTT and colony formation assays to measure cell viability and growth, Annexin V flow cytometry for apoptosis detection, and transwell migration assays for motility. In vivo syngeneic tumor models allow assessment of tumor growth kinetics. ChIP-qPCR can be employed to examine Brd7 complex occupancy at target promoters. For more information, please contact Ascent Research.