In Stock Cell Lines
Mus musculus (Mouse)
Liver
Adherent
The Slc3a2 Knockout Hepa 1-6 Cell Line is a CRISPR/Cas9-edited knockout line from mouse hepatoma Hepa 1-6 cells, with targeted disruption of Slc3a2 (CD98). Slc3a2 encodes the heavy chain of heterodimeric amino acid transporters that, with SLC7A5/SLC7A8, mediate large neutral amino acid uptake, activating mTORC1 via S6K and 4E-BP1. By also interacting with integrin ??1, Slc3a2 promotes FAK/ERK signaling and adhesion. This model aids investigation of amino acid?Cdependent growth, integrin-mediated metastasis, and metabolic dependencies in liver cancer, using uptake assays, western blot, and migration studies.
GANAB Knockout SK-HEP-1 Polyclonal Cells
Cat. No. ARG16144
CHMP7 Knockout 143B Polyclonal Cells
Cat. No. ARG11832
NUDT9 Knockout Hela Polyclonal Cells
Cat. No. ARG7918
HNF4A Knockout HAP1 Polyclonal Cells
Cat. No. ARG22564
C1orf50 Knockout jurkat Polyclonal Cells
Cat. No. ARG41328
Rat Renal Epithelial Cell Medium
Cat. No. ARM0268
The Slc3a2 Knockout Hepa 1-6 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the mouse hepatoma Hepa 1-6 line, featuring targeted disruption of the Slc3a2 gene (CD98 heavy chain). This isogenic loss-of-function model enables investigation of Slc3a2-dependent processes in a liver cancer context, providing a critical resource for biomedical research.
Hepa 1-6 cells, originating from a spontaneous BW7756 hepatoma in C57L/J mice, retain hepatocyte-like metabolic and synthetic functions. Widely used as a syngeneic model for hepatocellular carcinoma, these cells provide a physiologically relevant platform for studying liver tumor biology and therapeutic interventions in immunocompetent hosts.
Slc3a2 encodes the heavy chain of heterodimeric amino acid transporters, associating with light chains SLC7A5 (LAT1) and SLC7A8 (LAT2) to mediate cellular uptake of large neutral amino acids. This amino acid influx activates mTORC1 signaling via Rag GTPases and Rheb, leading to phosphorylation of downstream effectors S6K and 4E-BP1. Slc3a2 also interacts with integrin ??1 and galectin-3 to promote focal adhesion kinase (FAK) signaling, ERK1/2 activation, and cell adhesion. Expression is regulated by oncogenic transcription factors MYC and HIF1A, as well as cytokines (TNF??) and growth factors (EGF), positioning Slc3a2 at the intersection of nutrient sensing and growth factor signaling.
In hepatocellular carcinoma, Slc3a2 overexpression drives proliferation, migration, and metastasis through dysregulated amino acid uptake and integrin signaling. Disrupting Slc3a2 in Hepa 1-6 cells allows dissection of its role in amino acid?Cdependent mTORC1 activation and adhesion-mediated oncogenic signals, offering insights into metabolic dependencies of liver cancer progression and identifying vulnerabilities for intervention.
This knockout cell line supports studies on amino acid transport using radiolabeled uptake assays, mTORC1 pathway analysis by western blot (p-S6K, p-4E-BP1), and surface CD98 detection by flow cytometry. Functional assays include Boyden chamber migration/invasion and proliferation measurements (MTS/BrdU). Researchers can further explore Slc3a2?CLAT1 interaction via co-immunoprecipitation and conduct rapamycin sensitivity or RNA-seq experiments. The model is ideal for investigating immunometabolism, drug resistance, and therapeutic targeting in liver cancer. For additional information or to request a quote, please contact Ascent Research.
