The DPP7 Knockout Huh-7 Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal population of Huh-7 cells harboring disruption of the DPP7 gene. This polyclonal knockout model provides a heterogeneous pool of cells with DPP7 loss-of-function, enabling robust functional studies without the selection bottleneck of single-cell clones. The CRISPR/Cas9 system was used to introduce targeted gene disruption, generating a versatile loss-of-function model suitable for apoptosis and protein turnover research.
Huh-7 cells are a well-differentiated hepatocellular carcinoma line originally derived from a male liver tumor. These epithelial cells serve as a widely employed model for hepatic cancer biology, drug metabolism, and liver disease research. Their stable growth characteristics and retention of hepatocyte-specific functions make them an ideal host for gene-targeting experiments aimed at dissecting oncogenic mechanisms and drug response pathways in a liver-specific context.
DPP7 encodes a cytoplasmic serine protease that functions as a proline-specific dipeptidyl aminopeptidase, removing N-terminal dipeptides from peptides with Pro or Ala at the penultimate position. It is involved in cytoplasmic peptide catabolism downstream of the ubiquitin-proteasome system and is regulated by cell quiescence signals and potentially by p53 and stress pathways. DPP7 activity influences apoptosis by cleaving substrates that include apoptotic regulatory proteins, such as XIAP and caspases, thereby modulating the balance between pro- and anti-apoptotic factors like BAX and BCL-2. Additionally, DPP7 indirectly interacts with proteasome components and may associate with molecular chaperones such as HSP70, forming a network that integrates protein degradation with cell death signaling.
In hepatocellular carcinoma, aberrant protein turnover and apoptosis evasion contribute to chemoresistance and tumor progression. Disruption of DPP7 in Huh-7 cells provides a physiologically relevant model to dissect its role in modulating chemosensitivity, particularly through its effects on caspase activation and apoptotic substrate processing. This polyclonal knockout population captures the natural cellular variability of gene targeting, making it valuable for studying population-level responses and for screening applications where clonal homogeneity is not required.
This product is ideally suited for investigating DPP7 function in apoptosis regulation and drug resistance in liver cancer. Researchers can employ a variety of assays, such as Western blotting for protein expression analysis, Caspase-3 activity assays to assess apoptosis initiation, Annexin V staining for apoptotic cell quantification, and MTS drug sensitivity assays to evaluate chemotherapeutic response. Furthermore, cell cycle analysis and RT-qPCR can be used to examine proliferative changes and transcriptional profiles. Together, these approaches enable rigorous validation of DPP7 as a therapeutic target. For additional details, please contact Ascent Research.
