The KLF4 Knockout 769-P Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population generated by targeted disruption of the KLF4 gene in the human renal cell carcinoma line 769-P. This polyclonal product provides a heterogeneous loss-of-function model for studying KLF4-mediated transcriptional regulation without clonal isolation, preserving population-level genetic diversity typical of tumor cell mixtures.
The 769-P host cell line was established from a primary clear cell renal cell adenocarcinoma and maintains key features of tumorigenic renal epithelial cells. These adherent cells exhibit characteristic epithelial morphology and are widely employed in renal cancer research as a model for clear cell renal cell carcinoma, enabling investigation of oncogenic signaling, metastatic behavior, and drug sensitivity in a clinically relevant cellular context.
KLF4 is a zinc-finger transcription factor that binds GC-rich promoter elements to activate or repress target genes. In epithelial cells, KLF4 promotes cell cycle arrest by upregulating CDKN1A (p21) and maintains epithelial identity through transcriptional activation of CDH1 (E-cadherin), while suppressing mesenchymal markers such as VIM (vimentin). KLF4 activity is modulated by upstream regulators including TGF-??, BMPs, Wnt ligands, EGF, and p53, and it physically interacts with co-regulators like SMAD3, EP300 (p300), and CTNNB1 (??-catenin). Through these interactions, KLF4 integrates signals from TGF-??/SMAD, Wnt/??-catenin, p53, and MAPK pathways to control cell proliferation, differentiation, and epithelial-mesenchymal transition (EMT).
In 769-P renal carcinoma cells, KLF4 is thought to exert context-dependent tumor-suppressive functions; its knockout may relieve growth inhibition and promote EMT, thereby enhancing tumorigenic potential. This model thus serves as a valuable tool to dissect how loss of KLF4 shifts the balance from epithelial homeostasis toward a more invasive, mesenchymal phenotype. It allows researchers to study the consequences of KLF4 ablation on cell cycle checkpoints, apoptosis resistance, and migratory capacity within the genetic background of clear cell renal cell carcinoma.
The KLF4 Knockout 769-P Polyclonal Cells are well-suited for a range of applications including functional analysis of KLF4 in renal cancer, tumor suppressor mechanism studies, EMT assays, drug resistance profiling, and signaling pathway dissection. Representative assays include Western blot and RT-qPCR for KLF4 and its targets (e.g., p21, E-cadherin), ChIP-qPCR for promoter occupancy, proliferation (CCK-8), transwell migration/invasion, apoptosis (Annexin V), cell cycle flow cytometry, RNA-seq transcriptome profiling, and co-immunoprecipitation for protein interactions. For additional information or technical support, please contact Ascent Research.
