The HTRA1 Knockout NCI-H1703 Polyclonal Cells product provides a polyclonal population of NCI-H1703 cells in which the HTRA1 gene has been disrupted through CRISPR/Cas9-mediated genome editing. This heterogeneous knockout model eliminates functional HTRA1 protein expression across the cell population, generating a powerful loss-of-function tool for investigating HTRA1-dependent regulatory mechanisms in a lung squamous cell carcinoma background. The polyclonal format preserves genetic diversity while enabling robust functional studies that do not require clonal isolation, making it suitable for high-throughput screening and population-level analyses of gene ablation effects.
NCI-H1703 is a well-characterized human non-small cell lung cancer cell line derived from a lung squamous cell carcinoma patient. As an adherent epithelial cell line with defined growth properties, NCI-H1703 serves as a clinically relevant model for studying the molecular pathology of squamous cell lung carcinoma, including processes such as invasion, metastasis, and therapeutic resistance. Its TP53 and KRAS wild-type status, along with its origin from a primary tumor site, provides a physiologically relevant context for dissecting the contributions of tumor suppressor genes and oncogenic pathways in this aggressive cancer subtype.
HTRA1 encodes a secreted serine protease that functions as a critical antagonist of TGF-?? signaling by cleaving and inactivating TGF-?? family ligands, thereby modulating downstream cascades. The protease is regulated by upstream factors such as TGF-??, EGF, and cellular stress signals, and it targets substrates including fibronectin, type II collagen, and the amyloid precursor protein. Through these interactions, HTRA1 dampens signaling through the TGFBR1?CSMAD2/3 axis while also influencing pathways involving MAPK1 and CTNNB1, thereby integrating extracellular matrix remodeling with control of cell proliferation, migration, and apoptosis. Its interaction with PDGF and other extracellular matrix proteins further extends its regulatory network.
In the NCI-H1703 squamous cell carcinoma context, disruption of HTRA1 removes a key negative regulator of TGF-?? activity, which is expected to enhance the oncogenic potential of TGF-?? signaling, promoting epithelial-mesenchymal transition, extracellular matrix remodeling, and pro-survival phenotypes. HTRA1 loss is implicated in the progression of multiple cancer types, including lung, ovarian, and gastric carcinomas, and its inactivation correlates with increased migratory and invasive capacity. This knockout model therefore allows researchers to mechanistically dissect how loss of HTRA1-mediated proteolysis contributes to the aggressive behavior of non-small cell lung cancer cells and their response to microenvironmental cues.
The HTRA1 Knockout NCI-H1703 Polyclonal Cells are ideally suited for a range of functional assays, including Western blotting and RT-qPCR to confirm target disruption, TGF-?? signaling reporter assays to measure pathway activation, and migration and invasion assays to assess metastatic potential. This model enables investigations into cancer metastasis, drug resistance, fibrosis, and angiogenesis, as well as the interplay between TGF-??, MAPK, and Wnt signaling in lung squamous cell carcinoma. For further technical details or customized support, please contact Ascent Research to discuss how this knockout model can be integrated into your experimental workflows.
