The APOBEC3C Knockout PaTu 8988t Polyclonal Cells product provides a polyclonal population of PaTu 8988t cells with CRISPR/Cas9-mediated disruption of the APOBEC3C gene. This pool of edited cells enables loss-of-function studies without requiring single-cell cloning, preserving population-level heterogeneity.
The PaTu 8988t cell line originates from a liver metastasis of a human pancreatic ductal adenocarcinoma, displaying epithelial morphology and carrying wild-type KRAS and mutant TP53. This model is well-suited for investigating mechanisms of metastatic progression and therapeutic resistance in pancreatic cancer.
APOBEC3C encodes a cytidine deaminase that catalyzes C-to-T transitions in single-stranded DNA, contributing to both innate antiviral immunity and cancer-associated mutagenesis. Its expression is potently induced by type I and II interferons through the JAK-STAT pathway, involving receptors IFNAR1/IFNAR2, kinases JAK1 and TYK2, and the transcription factor complex ISGF3 (STAT1/STAT2/IRF9). Additionally, inflammatory cytokines such as TNF-alpha and IL-6 activate NF-??B, which further upregulates APOBEC3C transcription. Once expressed, APOBEC3C interacts with single-stranded DNA, replication protein A (RPA), and other APOBEC3 family members, and can edit viral genomes including HIV-1, where it is counteracted by the viral protein Vif. Downstream mutagenic targets include critical cancer genes such as TP53, PIK3CA, KRAS, and c-MYC, linking APOBEC3C activity to tumor heterogeneity and drug resistance.
In the PaTu 8988t background, which harbors a TP53 mutation and lacks oncogenic KRAS, APOBEC3C disruption offers a powerful tool to dissect endogenous mutation processes and their contribution to pancreatic cancer progression. This polyclonal knockout model allows investigators to assess how loss of APOBEC3C affects genomic stability, drug sensitivity, and the emergence of resistance mechanisms in a metastatic pancreatic adenocarcinoma context.
This knockout cell population is ideally suited for functional genomics studies examining APOBEC3C-dependent mutagenesis in pancreatic cancer, including whole exome sequencing to identify mutation signatures and colony formation assays to assess clonogenic survival after genotoxic stress. Researchers can employ cytotoxicity assays to evaluate how APOBEC3C loss alters sensitivity to chemotherapeutic agents, and RT-qPCR or western blotting to confirm changes in APOBEC3C expression. Additionally, these cells are compatible with HIV-1 infectivity assays to explore APOBEC3C-mediated viral restriction. For further information or to inquire about this product, please contact Ascent Research.
