The ID3 Knockout PaTu 8988t Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed to eliminate functional expression of the ID3 gene. This polyclonal population originates from the human pancreatic ductal adenocarcinoma cell line PaTu 8988t and has been engineered using CRISPR/Cas9-mediated gene disruption to create a heterogeneous pool of cells with target-gene loss of function. The resulting knockout model provides a powerful tool for dissecting the role of ID3 in pancreatic cancer biology, enabling robust investigation of signaling pathways and cellular processes in a disease-relevant context without relying on single-cell clonal selection.
PaTu 8988t is a pancreatic ductal adenocarcinoma (PDAC) cell line established from a liver metastasis of a human pancreatic tumor. It is widely used as an in vitro model for studying PDAC progression, metastasis, and therapeutic responses. This adherent epithelial cell line retains key molecular features of primary pancreatic cancer, including activation of TGF-?? and BMP signaling cascades, making it an ideal host for exploring the functional impact of ID3 ablation in a metastatic background.
ID3 functions as a dominant-negative inhibitor of basic helix-loop-helix (bHLH) transcription factors, particularly E-proteins such as TCF3/E2A, TCF12/HEB, and TCF4/E2-2. By sequestering these transcription factors, ID3 prevents their binding to E-box sequences and thereby represses transcription of downstream targets, including cell cycle regulators like CDKN1A/p21, CCND1, and MYC. ID3 expression is transcriptionally activated by multiple upstream signals, including TGF-??1 acting via the SMAD2/3/4 complex, BMP2/4 signaling through SMAD1/5/8, and Notch intracellular domain (NICD). Additionally, ID3 interacts with the retinoblastoma protein (RB), linking its regulatory network to cell cycle control. Disruption of ID3 de-represses E-protein activity, leading to altered transcription of genes controlling proliferation, differentiation, and apoptosis.
In the context of PaTu 8988t cells, knockout of ID3 is expected to significantly impact the delicate balance between growth-promoting and growth-inhibitory signals. PDAC cells often exploit ID3 upregulation to sustain unchecked proliferation and evade apoptosis. Removing ID3 function may restore E-protein-mediated tumor-suppressive programs, providing insights into the mechanistic underpinnings of pancreatic tumorigenesis. This model enables researchers to dissect how ID3 loss modulates responses to TGF-?? and BMP ligands, with implications for understanding metastatic competence and drug resistance in pancreatic adenocarcinoma.
This polyclonal knockout cell product is suited for a broad range of research applications, including detailed analysis of TGF-??/BMP and Notch signaling dynamics, cell cycle regulation studies, and apoptosis profiling. Typical assays include Western blotting for ID3 and downstream targets, RT-qPCR for transcript changes, proliferation assays (MTT, BrdU), flow cytometry for cell cycle and Annexin V apoptosis staining, migration/invasion assays, and E-box reporter assays. Co-immunoprecipitation with E-proteins and phospho-SMAD analysis further enable biochemical dissection of signaling complexes. This model also supports transcriptome-wide profiling via RNA-seq and drug screening efforts. For additional details or to inquire about this product, please contact Ascent Research.
