In Stock Cell Lines
Homo sapiens (Human)
Liver
Adherent
The HIF1A Knockout Huh-7 Cell Line is a CRISPR/Cas9-edited knockout cell line that disrupts the HIF1A gene encoding hypoxia-inducible factor 1-alpha (HIF-1??) in the Huh-7 human hepatocellular carcinoma background. This model enables loss-of-function studies of HIF-1??, a central transcription factor that mediates adaptive responses to low oxygen by regulating genes such as VEGF and GLUT1. Under hypoxia, HIF-1?? stabilization drives angiogenesis and glycolysis through targets like VEGF and GLUT1. This knockout line suits hypoxia research, HCC modeling, and anti-angiogenic drug validation. For inquiries, contact Ascent Research.
CNOT10 Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG17524
P4HA2 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG17288
HTR3C Knockout HAP1 Polyclonal Cells
Cat. No. ARG22659
IL3 Knockout Hela Polyclonal Cells
Cat. No. ARG36099
DTD1 Knockout HGC-27 Polyclonal Cells
Cat. No. ARG39870
Slc39a1 Knockout Huh-7 Cell Line
Cat. No. ARG0450
The HIF1A Knockout Huh-7 Cell Line is a CRISPR/Cas9-edited knockout cell line designed to disrupt the HIF1A gene in the Huh-7 human hepatocellular carcinoma background. This loss-of-function model enables precise investigation of hypoxia-inducible factor 1-alpha (HIF-1??), a master transcriptional regulator of the cellular hypoxic response. The knockout line provides a powerful tool for dissecting both hypoxia-dependent and hypoxia-independent functions of HIF-1?? in liver cancer biology, metabolic adaptation, and signal transduction.
The Huh-7 cell line is a well-differentiated hepatocellular carcinoma line isolated from a liver tumor of a 57-year-old Japanese male. It is widely utilized as a model for liver cancer, hepatocyte metabolism, and drug metabolism studies, and is permissive for hepatitis C virus replication. Huh-7 cells retain key hepatic functions and signaling networks, making them an appropriate host for studying oncogenic mechanisms, metabolic reprogramming, and therapeutic responses in a clinically relevant epithelial context.
HIF1A encodes the oxygen-sensitive alpha subunit of the HIF-1 transcription factor. In normoxia, HIF-1?? is hydroxylated by prolyl hydroxylases (PHD1?C3), leading to VHL ubiquitin ligase recognition and proteasomal degradation. Factor inhibiting HIF (FIH) also suppresses coactivator binding. Under hypoxia, hydroxylation ceases, HIF-1?? accumulates, dimerizes with HIF-1?? (ARNT), and recruits p300/CBP to transactivate genes via hypoxia response elements (HREs). Key targets include VEGF, GLUT1, PDK1, and HK2, which promote angiogenesis and glycolytic metabolism. HIF-1?? activity is further modulated by upstream signals such as EGF, IGF-1, PI3K, Akt, mTOR, MAPK, reactive oxygen species, and inflammatory cytokines (TNF-??, IL-1??).
In hepatocellular carcinoma, HIF-1?? is frequently overexpressed due to intratumoral hypoxia and oncogenic pathway activation, driving angiogenesis, metabolic switch to glycolysis, and resistance to therapy. The HIF1A knockout in Huh-7 cells therefore creates a critical model to examine how loss of HIF-1?? impacts hypoxic adaptation, proliferation, migration, and drug sensitivity in a well-differentiated liver cancer line. This enables the elucidation of HIF-1????s role in processes such as sorafenib resistance and altered hepatic drug metabolism, while also permitting dissection of crosstalk with the PI3K-Akt and mTOR pathways.
This knockout line supports applications such as hypoxia chamber exposure coupled with Western blot detection of HIF-1?? stabilization, RT-qPCR of target genes (VEGF, GLUT1), HRE-luciferase assays, and Seahorse glycolysis stress tests. Additional phenotypic assays include migration, invasion, and clonogenic survival under low oxygen. The model is a versatile tool for hypoxia research, hepatocellular carcinoma studies, anti-angiogenic drug validation, and metabolic reprogramming investigations. For further details, please contact Ascent Research.
