The BATF3 Knockout LoVo Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function analyses of the BATF3 transcription factor in a human colorectal adenocarcinoma background. This format provides a genetically heterogeneous model system, avoiding clonal biases and enabling robust population-level phenotypic readouts. These cells serve as a versatile tool for investigating BATF3-dependent mechanisms in colorectal cancer without the confounding effects of monoclonal selection.
The LoVo cell line is a human colorectal adenocarcinoma originally derived from a metastatic lymph node of a colon adenocarcinoma patient. It displays epithelial morphology with mutations in APC and KRAS, serving as a clinically relevant model for colorectal cancer research. LoVo cells exhibit reproducible growth, tumorigenicity in xenografts, and sensitivity to chemotherapeutic agents such as 5-fluorouracil and oxaliplatin.
BATF3 is a basic leucine zipper transcription factor that acts as a master regulator of conventional dendritic cell development, particularly the CD8??+ and CD103+ cross-presenting subsets. It forms heterodimers with IRF8 or IRF4 and cooperates with JUN, BATF, and FOS to regulate gene expression. Upstream, BATF3 is induced by interferon-gamma via JAK1/2?CSTAT1 and by FLT3 ligand through STAT5, integrating signals from GM-CSF and NFIL3. Downstream, it activates ID2, IRF8, ZEB2, IL12B, and CXCL9, and drives expression of antigen presentation components TAP1/2 and MHC class I, linking TLR?CMyD88 innate signaling to adaptive immunity.
In LoVo colorectal cancer cells, BATF3 knockout allows dissection of tumor-intrinsic functions, potentially influencing immunogenic cell death, cytokine secretion, and antigen presentation. Loss of BATF3 may alter the secretome and chemokine-mediated immune cell recruitment, impacting the tumor microenvironment. This model is relevant for studying how BATF3 activity affects sensitivity to immunogenic chemotherapy and immune checkpoint blockade, providing a platform for mechanistic studies of colorectal cancer progression and therapeutic response.
Typical applications include profiling gene expression via RNA-seq and RT-qPCR, protein analysis by Western blotting and immunofluorescence, and MHC-I surface assessment by flow cytometry. Functional assays such as co-culture with T cells, migration/invasion, and apoptosis assays enable study of immune?Ccancer cell interactions. These cells are suitable for drug sensitivity screens with 5-fluorouracil and oxaliplatin and for investigating immunogenic cell death. For further information, contact Ascent Research.
