The BATF3 Knockout PaTu 8988t Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout population targeting the BATF3 gene in the human pancreatic ductal adenocarcinoma cell line PaTu 8988t. This heterogeneous cell pool harbors diverse loss?of?function mutations, offering a robust and versatile gene disruption model while maintaining genetic diversity and reducing clonal selection artifacts. The polyclonal format is ideal for studying BATF3 function in a tumorigenic context without single?cell?derived biases.
The parental PaTu 8988t line was established from a liver metastasis of a pancreatic adenocarcinoma and carries oncogenic KRAS G12V and TP53 mutations, reflecting common driver alterations in pancreatic cancer. This well?characterized tumorigenic model is widely employed to investigate pancreatic ductal adenocarcinoma biology, including metastatic dissemination, chemoresistance, and tumor?Cimmune cell cross?talk.
BATF3 encodes a basic leucine zipper transcription factor that heterodimerizes with JUN and FOS to regulate gene expression programs critical for immune cell differentiation. Its activity is induced by Flt3L and GM?CSF through STAT3 and STAT5 signaling, leading to transcriptional activation of downstream targets such as IRF8, ID2, IL12b, CCL5, and CXCL10. BATF3 is essential for the terminal differentiation of cross?presenting CD8??+ and CD103+ conventional dendritic cells (cDCs), which are specialized in priming CD8+ T cells and producing IL?12. The BATF3?CJUN complex cooperates with IRF4 and IRF8 to orchestrate cDC lineage specification, establishing a bridge between innate immune detection and adaptive immunity.
In the context of pancreatic adenocarcinoma, BATF3 disruption in PaTu 8988t cells provides a unique opportunity to probe the function of this transcription factor beyond the hematopoietic compartment. Loss of BATF3 may directly alter expression of immunomodulatory cytokines and chemokines such as IL?12, CCL5, and CXCL10, potentially reshaping the tumor microenvironment and influencing immune cell infiltration. This model enables dissection of BATF3?dependent transcriptional networks within cancer cells and their contribution to tumor progression, immune evasion, and responsiveness to immunotherapeutic interventions.
This polyclonal knockout population is amenable to a variety of experimental approaches, including flow cytometric analysis of immune markers, T cell proliferation and activation assays, ELISA?based cytokine measurement, Western blot, and RT?qPCR for transcriptional profiling. The model is particularly well?suited for in vivo tumor transplantation studies to assess the role of tumor?intrinsic BATF3 in primary tumor growth, metastatic spread, and response to checkpoint blockade or vaccine?based immunotherapies. Key research applications include tumor immunology, dendritic cell development, autoimmune disease mechanisms, and preclinical evaluation of immunotherapies. For additional information, please contact Ascent Research.
