The AGGF1 Knockout T-47D Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the human breast adenocarcinoma cell line T-47D, engineered to disrupt the AGGF1 gene. This polyclonal knockout model provides a heterogeneous loss-of-function system to investigate AGGF1-dependent cellular processes without clonal selection, reflecting the genetic diversity inherent in tumor cell populations. The gene disruption is achieved via CRISPR/Cas9-mediated genome editing, generating a mixed pool of cells with targeted mutations in AGGF1, enabling robust functional studies in angiogenesis and cancer biology.
T-47D is an epithelial cell line isolated from a pleural effusion of a ductal carcinoma, characterized by estrogen receptor (ER)-positive, progesterone receptor (PR)-positive, and HER2-negative status. This hormone-responsive line serves as a widely used model for luminal A breast cancer, retaining key signaling pathways dependent on estradiol and progesterone. Its well-differentiated epithelial morphology and expression of hormone receptors make it particularly suitable for studying endocrine-related tumor biology and the interplay between angiogenic factors and hormone signaling in breast cancer progression.
AGGF1 encodes an angiogenic factor with a forkhead-associated domain and a G-patch domain, functioning as a positive regulator of endothelial cell proliferation, adhesion, and vascular development. It is transcriptionally upregulated by TNF and HIF1A in response to inflammatory and hypoxic stimuli, linking microenvironmental cues to angiogenic output. Downstream, AGGF1 promotes activation of AKT1 and MAPK1/3 (ERK2/1), leading to increased expression of CCND1 (Cyclin D1) and suppression of CDKN1A (p21), thereby driving cell cycle progression and proliferation. Additionally, AGGF1 interacts with GATA2, HDAC1, and SMAD4, implicating epigenetic and transcriptional regulatory complexes in its angiogenic function. Through these pathways, AGGF1 modulates VEGFA expression and amplifies pro-angiogenic signals, positioning it as a key node in vascular homeostasis and tumor angiogenesis.
In the ER-positive T-47D background, AGGF1 knockout is expected to impair the cell-autonomous angiogenic potential and reduce proliferation, consistent with its role in AKT and ERK signaling. Given that T-47D cells retain hormone responsiveness, this model allows dissection of how AGGF1 intersects with estrogen-driven growth and survival pathways. Loss of AGGF1 may attenuate tumor-stroma crosstalk by diminishing paracrine angiogenic signals, offering a platform to study tumor microenvironment remodeling in hormone-dependent breast cancer. Moreover, as AGGF1 is implicated in DNA damage repair, knockout T-47D cells may exhibit sensitization to genotoxic stress, providing a tool to explore therapeutic vulnerabilities in breast malignancies.
Typical applications include western blotting and RT-qPCR to confirm AGGF1 disruption, functional assays such as tube formation, MTS/MTS proliferation, and migration/invasion to assess angiogenic and metastatic capacities, and phospho-specific analysis of AKT and ERK to interrogate downstream signaling. Transcriptomic profiling via RNA-seq can reveal global gene expression changes resulting from AGGF1 loss. This polyclonal pool is ideal for studying AGGF1-mediated angiogenesis in breast cancer, evaluating anti-angiogenic therapies, and performing functional genomics of vascular development. For additional information and customization options, please contact Ascent Research.
