The HIVEP1 Knockout NCI-H1975 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the HIVEP1 gene. This product comprises a heterogeneous pool of NCI-H1975 cells that have undergone CRISPR/Cas9-mediated gene disruption at the HIVEP1 locus, generating a mixed population of knockout alleles without single-cell clonal isolation. The resulting polyclonal knockout cells provide a physiologically relevant model to dissect the role of the HIVEP1 transcription factor in immune-related transcriptional programs and cancer cell signaling.
The NCI-H1975 cell line is a well-established human non-small cell lung adenocarcinoma (NSCLC) model derived from an epithelial tumor. These cells exhibit characteristics of lung adenocarcinoma and are widely utilized in cancer biology research, particularly for investigating oncogenic signaling, drug resistance, and tumor-immune interactions. As an adherent epithelial line, NCI-H1975 retains key features of the parental tumor, making it suitable for functional studies of transcription factors like HIVEP1 that may influence tumor cell behavior and inflammatory responses.
HIVEP1 (human immunodeficiency virus type I enhancer binding protein 1), also known as ZAS1 or PRDII-BF1, is a large zinc finger transcription factor that binds cis-regulatory elements to modulate gene expression. It is activated by pro-inflammatory stimuli, including tumor necrosis factor (TNF), interleukin-1?? (IL-1??), and Toll-like receptor (TLR) ligands. Upon stimulation, HIVEP1 interacts with NF-kB subunits and I??B??, integrating into the IKK?CI??B???CNF-kB signaling axis. HIVEP1 transcriptionally regulates downstream targets such as the HIV-1 enhancer, major histocompatibility complex (MHC) class I genes, and various NF-kB target genes encoding cytokines and chemokines. Through these interactions, HIVEP1 fine-tunes NF-kB-dependent transcriptional responses, positioning it as a critical modulator of immune and inflammatory gene expression.
In the NCI-H1975 lung adenocarcinoma background, disruption of HIVEP1 is expected to perturb NF-kB-mediated transcriptional programs, potentially altering the expression of inflammatory cytokines, chemokines, and immune-related surface molecules. Given the role of NF-kB signaling in cancer cell survival, proliferation, and immune evasion, HIVEP1 knockout in this model may reveal context-specific dependencies of NSCLC cells on inflammatory pathways. The polyclonal nature of the knockout population better mimics the genetic heterogeneity observed in tumors and avoids clonal artifacts associated with single-cell-derived knockout lines, thereby providing a more robust system for studying HIVEP1 function in a cancer setting.
Researchers can employ these polyclonal HIVEP1 knockout cells to investigate mechanisms of immune evasion in non-small cell lung cancer, delineate the transcriptional regulation of NF-kB target genes, and functionally analyze inflammatory signaling networks. Representative experimental approaches include western blotting for HIVEP1 and phospho-NF-kB to assess pathway activation, RT-qPCR to quantify downstream targets, NF-kB luciferase reporter assays to measure transcriptional activity, and cytokine ELISA following TNF stimulation to evaluate secretory responses. Additionally, migration and invasion assays, as well as drug sensitivity profiling, can be performed to link HIVEP1-dependent signaling to cellular phenotypes and therapeutic vulnerabilities. For further information, please contact Ascent Research.
