The BATF3 Knockout HGC-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 human gastric carcinoma cell line, engineered to disrupt the BATF3 gene locus. This polyclonal knockout pool provides a heterogeneous collection of edited cells with targeted disruption of BATF3, facilitating loss-of-function studies in gastric cancer contexts without clonal selection. The product is supplied as a polyclonal cell population to preserve genetic diversity and reduce clonal artifacts, making it suitable for experiments requiring representation of multiple editing outcomes.
HGC-27 is an undifferentiated gastric carcinoma cell line established from lymph node metastasis, exhibiting an epithelial phenotype and widely employed in gastric cancer research. It serves as a relevant model for studying metastatic gastric cancer biology, including tumor cell invasiveness, drug response, and tumor-immune interactions. The lymph node origin underscores its utility in investigating mechanisms of lymphatic spread and tumor microenvironmental crosstalk. Researchers utilize HGC-27 to explore oncogenic signaling, apoptosis, and epithelial-mesenchymal transition, with BATF3 knockout adding a layer of immunological relevance.
BATF3 encodes a basic leucine zipper (bZIP) transcription factor critical for dendritic cell development and function, particularly conventional dendritic cells type 1 (cDC1). It operates within the AP-1 transcription factor network, forming heterodimers with JUN, FOS, and other bZIP proteins to regulate gene expression. BATF3 is transcriptionally activated downstream of FLT3L-FLT3-STAT5 signaling and IRF8, a master regulator of dendritic cell specification. BATF3, in turn, promotes expression of ID2, XCR1, and IL-12, essential for cross-presentation and Th1 polarization. Its activity shapes anti-tumor immunity by enhancing CD8+ T cell priming through cDC1-mediated antigen presentation. In the context of gastric cancer, BATF3 may influence immune surveillance by modulating dendritic cell recruitment and function.
Disruption of BATF3 in HGC-27 cells is expected to abrogate BATF3-dependent transcriptional programs intrinsic to tumor cells, potentially altering cytokine secretion, antigen presentation machinery, and immune-regulatory molecule expression. This model may impact tumor cell interactions with dendritic cells and CD8+ T cells, consequently influencing anti-tumor immune responses. The polyclonal knockout population enables study of BATF3 loss in gastric cancer cells without clonal selection pressures, mimicking a heterogeneous tumor setting. It provides a tool to dissect how BATF3 deficiency in malignant epithelial cells contributes to immune evasion, tumor progression, or altered sensitivity to immunotherapeutic agents. Given the role of BATF3 in dendritic cell biology and cross-presentation, this model also facilitates co-culture experiments assessing dendritic cell function in the tumor microenvironment.
Typical research applications include investigation of cancer immunology, dendritic cell biology, and tumor microenvironment dynamics. The cells can be used in co-culture assays with dendritic cells and T cells to evaluate cross-presentation and T cell activation, in migration and invasion assays to study metastatic behavior, and in drug sensitivity screens to assess responses to chemotherapeutics or immunomodulators. Methodologies such as Western blotting, RT-qPCR, RNA-seq, and flow cytometry enable analysis of BATF3 target gene expression and immune surface markers. Cytokine ELISA can quantify secreted factors like IL-12. This knockout model supports target validation for immunotherapies and mechanistic studies of gastric cancer immune escape. For additional details, please contact Ascent Research.
