The KLF7 Knockout HCT 116 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout population derived from the HCT 116 human colorectal carcinoma cell line, featuring targeted disruption of the KLF7 gene. KLF7 encodes a Kr??ppel-like zinc-finger transcription factor involved in cell differentiation, neuronal development, adipogenesis, and tumor suppression. This polyclonal knockout model provides a heterogeneous loss-of-function system, enabling robust analysis of KLF7-dependent transcriptional networks without introducing clonal selection artifacts.
HCT 116 is an epithelial colorectal carcinoma cell line derived from an adult male, characterized by an activating KRAS G13D mutation and defective DNA mismatch repair (dMMR) that results in microsatellite instability (MSI). These genetic hallmarks establish HCT 116 as a validated model for colorectal cancer research, particularly for investigating oncogenic KRAS-driven signaling and genomic instability. The cell line retains wild-type TP53 and functional apoptotic machinery, making it suitable for tumor suppressor gene studies and drug discovery.
KLF7 functions as a transcriptional regulator that integrates upstream signaling inputs. The transcription factor SP1 and the ERK/MAPK cascade, activated downstream of neurotrophin signaling (NGF/TrkA/RAS/ERK/CREB), induce KLF7 expression, while TGF-?? signaling modulates its activity. KLF7 interacts with coregulators Sin3A, HDAC1, and p300/CBP to activate or repress target genes. It promotes transcription of CDKN1A (p21) and NTRK1 (TrkA), and represses CCND1 (cyclin D1) and BCL2, thereby enforcing cell cycle arrest and sensitizing cells to apoptosis.
Disruption of KLF7 in HCT 116 cells abrogates its transcriptional control over cell cycle inhibitors and apoptotic modulators, mirroring functional losses observed in advanced colorectal carcinomas. Reduced KLF7 activity is expected to downregulate p21, derepress cyclin D1, and increase BCL2 levels, accelerating G1/S transition, enhancing proliferation, and promoting survival. This polyclonal knockout population thus recapitulates key oncogenic processes driven by KLF7 deficiency in a background of mutant KRAS and mismatch repair defects, providing a powerful platform to study cooperative mechanisms in colorectal cancer progression and therapeutic resistance.
This KLF7 knockout cell pool supports a wide array of research applications, including tumor suppressor mechanism elucidation and colorectal cancer progression modeling. Researchers can identify transcriptional targets via RT-qPCR, confirm protein changes by western blotting for p21 and cyclin D1, and assess functional outcomes using proliferation (MTS), apoptosis (Annexin V), colony formation, and flow cytometry for cell cycle distribution. The model facilitates drug target validation aimed at restoring KLF7 function or targeting its downstream effectors. For additional information, contact Ascent Research.
