The HCFC1R1 Knockout NCI-H1703 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human NCI-H1703 lung adenocarcinoma cell line. This product offers a heterogeneous pool of cells carrying targeted disruptions in the HCFC1R1 (HPIP) gene, enabling loss-of-function studies without clonal selection biases. The cells are provided as a ready-to-use population, ideal for researchers investigating the molecular underpinnings of non-small cell lung cancer.
The NCI-H1703 parental cell line originates from a male patient with lung adenocarcinoma and serves as a well-characterized model of malignant lung epithelium. These adherent epithelial cells recapitulate key features of non-small cell lung cancer, including aberrant growth signaling and metastatic potential. The line is commonly employed in oncology research to dissect tumorigenic mechanisms and evaluate therapeutic interventions.
HCFC1R1 encodes a scaffold protein that forms complexes with the transcription factors PBX1 and HCFC1, thereby regulating gene expression programs critical for oncogenesis. It functions downstream of multiple upstream regulators, including TGF-??, estrogen, and microRNAs such as miR-148a and miR-200c, and transduces signals through the PI3K/AKT and MAPK/ERK cascades. Key pathway components, including PIK3CA, AKT1, MTOR, KRAS, RAF1, and MAPK1, mediate its pro-proliferative effects. The scaffold also interfaces with Wnt/??-catenin signaling via CTNNB1 and TGF-?? pathways through SMAD2, while interacting with ESR1, SRC, and the PI3K regulatory subunit to amplify mitogenic and survival signals. Downstream, HCFC1R1 promotes transcription of target genes such as BCL2, CCND1, MYC, SNAI1, MMP2, and MMP9, which collectively drive cell cycle progression, apoptosis resistance, and metastatic dissemination.
In non-small cell lung cancer, HCFC1R1 overexpression drives enhanced proliferation, survival, and migration, contributing to aggressive tumor behavior. The NCI-H1703 knockout model enables investigators to directly assess how loss of HCFC1R1 impacts these malignant phenotypes, including epithelial-mesenchymal transition and matrix degradation. By disrupting this oncogenic scaffold, researchers can decipher its role in modulating downstream effectors and signaling crosstalk in a lung adenocarcinoma context.
This polyclonal knockout product is suited for a range of experimental applications, including western blotting, RT-qPCR, and RNA-seq for expression profiling, as well as functional assays such as proliferation (MTS), migration (wound healing), invasion (Matrigel), and apoptosis (Annexin V). Additionally, the cells facilitate drug sensitivity testing, CHIP-qPCR for chromatin interactions, and immunofluorescence localization studies. These applications support target validation, pathway dissection, and preclinical drug development in lung cancer research. For further information or technical assistance, please contact Ascent Research.
