Genome-edited Cells
Liver
The KLF4 Knockout MHCC97-H Cell Line is a CRISPR/Cas9-edited knockout cell line generated from the highly metastatic MHCC97-H human hepatocellular carcinoma line. KLF4 is a tumor-suppressive transcription factor that regulates cell cycle, apoptosis, and epithelial-mesenchymal transition (EMT) by modulating targets such as p21 and E-cadherin, and through inhibition of Wnt/??-catenin and PI3K/AKT signaling. This knockout model in an aggressive liver cancer background is ideal for investigating KLF4's role in HCC metastasis, EMT, and tumor suppression. Applications include functional genomics, drug screening, and molecular mechanism studies using assays like Transwell migration, Annexin V apoptosis, and pathway activity analysis.
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The KLF4 Knockout MHCC97-H Cell Line is a CRISPR/Cas9-edited knockout cell line featuring targeted disruption of the KLF4 gene within the MHCC97-H human hepatocellular carcinoma host background. This stable loss-of-function model is supplied as a validated cell line and is designed to facilitate detailed functional studies of KLF4 in a metastatic liver cancer setting. The use of CRISPR/Cas9-mediated gene disruption enables robust knockout while preserving the genetic integrity of the host line.
The MHCC97-H cell line was established from the LCI-D20 metastatic human hepatocellular carcinoma and is recognized for its high invasive and metastatic potential. These cells exhibit aggressive motile and invasive behaviors, making them an ideal platform for examining mechanisms underlying HCC metastasis and for evaluating the role of tumor suppressor genes such as KLF4 in controlling these processes.
KLF4 is a zinc-finger transcription factor that orchestrates cell cycle arrest, apoptosis, differentiation, and maintenance of stemness. In hepatocellular carcinoma, KLF4 acts as a tumor suppressor by upregulating cyclin-dependent kinase inhibitors p21/CDKN1A and p27/CDKN1B and by suppressing Cyclin D1 expression. KLF4 also antagonizes epithelial-mesenchymal transition (EMT) through transcriptional activation of E-cadherin and repression of mesenchymal markers such as Snail, Vimentin, MMP2, and MMP9. Its activity is regulated by upstream signals including TGF-??1, p53, and AKT, and it functionally interacts with coregulators p300/CBP and HDAC1/2. KLF4 integrates diverse signaling cascades, notably inhibiting Wnt/??-catenin and PI3K/AKT pathways to exert its anti-proliferative and anti-metastatic effects.
In the highly metastatic MHCC97-H background, disruption of KLF4 is anticipated to potentiate proliferative capacity, suppress apoptosis, and enhance EMT-driven invasion. This knockout model thus provides a relevant cellular context to dissect how KLF4 loss cooperates with the endogenous aggressive phenotype, allowing exploration of downstream effectors such as ??-catenin, AKT, Smad2/3, and ERK in promoting HCC progression. Consequently, the KLF4 Knockout MHCC97-H Cell Line serves as a critical tool for deciphering the molecular interplay between KLF4 and pathways involved in hepatocellular carcinoma metastasis.
Researchers can employ this cell line to investigate tumor suppressor mechanisms, study EMT regulation, perform drug sensitivity screening, and analyze signaling pathway alterations. Compatible techniques include Western blotting, RT-qPCR, RNA-seq, ChIP-qPCR, immunofluorescence, flow cytometry, Transwell migration/invasion assays, wound healing assays, Annexin V apoptosis detection, and luciferase reporter assays. The model also supports co-immunoprecipitation and analysis of phospho-AKT/ERK changes. For further technical details or support, please contact Ascent Research.
