The KLF13 Knockout NCI-H1975 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population targeting the KLF13 gene in the NCI-H1975 human lung adenocarcinoma cell line. This product provides a loss-of-function model for studying the tumor-suppressive and regulatory roles of KLF13 in non-small cell lung cancer (NSCLC). The polyclonal population contains a heterogeneous mix of gene-disrupted cells generated by CRISPR/Cas9-mediated gene disruption, enabling robust analysis of KLF13-dependent phenotypes without clonal selection bias.
NCI-H1975 is a widely characterized human lung adenocarcinoma epithelial cell line derived from a non-small cell lung cancer patient. These cells harbor activating EGFR mutations L858R and T790M, which are key drivers of oncogenic signaling and acquired resistance to first-generation EGFR tyrosine kinase inhibitors. This genetic background makes NCI-H1975 an essential model for investigating EGFR-targeted therapies, drug resistance mechanisms, and tumor progression in lung adenocarcinoma.
KLF13 is a Kr??ppel-like transcription factor that binds GC-rich promoter elements to activate or repress transcription of genes involved in cell proliferation, differentiation, and apoptosis. In the TGF-beta signaling pathway, KLF13 functions downstream of TGFB1, SMAD2, and SMAD3, and transcriptionally regulates critical targets such as CCND1 (cyclin D1), CDKN1A (p21), and BCL2. It also interacts with co-regulators like SP1, CBP, and SIN3A to modulate gene expression. Through these interactions, KLF13 integrates signals from the TGFBR1?CSMAD2/3?CSMAD4 axis to control cell cycle arrest and apoptotic responses.
Disruption of KLF13 in NCI-H1975 cells is expected to impair TGF-beta-mediated growth inhibition, potentially enhancing tumorigenic potential and altering sensitivity to chemotherapeutic agents or targeted inhibitors. The EGFR-mutant background of this model provides a unique context to explore how KLF13 loss cooperates with oncogenic signaling in NSCLC, offering insights into tumor suppression and the molecular basis of drug resistance.
This KLF13 knockout model supports a broad range of research applications, including the study of tumor suppressor function, TGF-beta signaling network dynamics, and lung adenocarcinoma biology. Representative experimental approaches include western blotting for protein expression analysis, RT-qPCR and RNA-seq for transcriptomic profiling, and ChIP-qPCR for examining KLF13 target gene occupancy. Functional assays such as apoptosis, migration, and drug sensitivity studies (e.g., to EGFR inhibitors) enable phenotypic characterization. For further details or technical assistance, please contact Ascent Research.
