Genome-edited Cells
Liver
The GIHCG Knockout Huh-7 Cell Line is a CRISPR/Cas9-edited knockout cell line targeting the oncogenic lncRNA GIHCG in human Huh-7 hepatocellular carcinoma cells. GIHCG promotes liver cancer progression by recruiting PRC2 (EZH2/SUZ12) to silence tumor suppressors and by activating PI3K/AKT signaling, leading to upregulation of CCND1 and MMP9 and repression of CDH1, thereby driving EMT and metastasis. This loss-of-function model enables mechanistic studies of GIHCG's role in cell cycle regulation, migration, and invasion, with applications in anti-cancer drug screening, HCV?Chost interaction research, and tumor microenvironment signaling. Representative assays include RT-qPCR, western blotting for AKT1 and CCND1, and xenograft tumor models.
FGFR3 Knockout SW1353 Cell Line
Cat. No. ARG43856
Mark3 Knockout RAW 264.7 Polyclonal Cells
Cat. No. ARG12527
JAG1 Knockout MCF7 Polyclonal Cells
Cat. No. ARG36459
CBR4 Knockout jurkat Polyclonal Cells
Cat. No. ARG42736
FKBP15 Knockout MES-OV Polyclonal Cells
Cat. No. ARG6509
CNRIP1 Knockout Raji Polyclonal Cells
Cat. No. ARG1640
The GIHCG Knockout Huh-7 Cell Line is a precisely engineered CRISPR/Cas9-edited knockout cell line designed to disrupt expression of the long non-coding RNA GIHCG in the Huh-7 human hepatocellular carcinoma (HCC) epithelial cell line. This product provides a stable loss-of-function cellular model for dissecting the molecular mechanisms by which GIHCG contributes to liver cancer pathogenesis, allowing researchers to interrogate its roles in proliferation, migration, and invasion without the confounding effects of transient knockdown approaches.
Huh-7 is a widely utilized human HCC cell line originally isolated in 1982 from a liver tumor of a 57-year-old Japanese male. These cells exhibit typical epithelial morphology, retain hepatocyte-derived characteristics, and are permissive for hepatitis C virus (HCV) replication, making them a valuable system for studying both HCC biology and virus?Chost interactions. The cell line harbors mutations commonly associated with liver cancer and serves as a robust platform for investigating oncogenic signaling networks in a clinically relevant context.
GIHCG is an oncogenic lncRNA that drives HCC aggressiveness through dual mechanisms. It physically interacts with the Polycomb Repressive Complex 2 (PRC2) components EZH2 and SUZ12, recruiting the complex to target gene promoters and inducing H3K27 trimethylation-dependent transcriptional silencing of tumor suppressors. Additionally, GIHCG activates the PI3K/AKT pathway by enhancing AKT1 phosphorylation, leading to mTOR-mediated upregulation of Cyclin D1 (CCND1). Transcriptionally controlled by STAT3 and c-Myc, GIHCG also responds to gonadotropin hormones. It promotes epithelial-mesenchymal transition (EMT) by inducing Snail (SNAI1), N-cadherin (CDH2), and matrix metalloproteinase 9 (MMP9), while concurrently repressing E-cadherin (CDH1). GIHCG further interacts with DNA methyltransferase 1 (DNMT1), linking it to DNA methylation-dependent gene silencing.
In the Huh-7 background, disruption of GIHCG abrogates its oncogenic functions, providing a powerful tool to dissect the lncRNA’s contribution to HCC malignancy. Loss of GIHCG impairs PI3K/AKT pathway activity, attenuates cell cycle progression by downregulating CCND1, and reverses EMT by restoring CDH1 expression while reducing MMP9 and SNAI1. This knockout cell line thus enables precise investigation of how GIHCG integrates upstream signals from STAT3 and c-Myc with downstream epigenetic and signaling outputs, allowing researchers to evaluate resulting phenotypic changes in a genetically defined system.
The GIHCG Knockout Huh-7 Cell Line is ideally suited for advanced applications including mechanistic lncRNA studies via RIP-qPCR for EZH2 binding and ChIRP-seq for genome-wide target identification, functional assays such as CCK-8 proliferation, Transwell migration/invasion, and western blotting for key pathway components (e.g., AKT1, CCND1, CDH1, SNAI1), anti-cancer drug screening targeting the PI3K/AKT/mTOR axis or EMT, and xenograft tumor growth models for in vivo metastasis research. It also facilitates investigation of HCV replication and tumor microenvironment signaling. For custom applications or further information, please contact Ascent Research.
