SIRT7 Knockout Hep-G2 Cell Line

The SIRT7 Knockout Hep-G2 Cell Line is a CRISPR/Cas9-edited knockout cell line designed for loss-of-function studies of the SIRT7 gene in a human hepatic epithelial environment. This product provides targeted disruption of SIRT7 using CRISPR/Cas9 genome editing, allowing researchers to dissect SIRT7-dependent signaling networks. Originating from the Hep-G2 hepatocellular carcinoma line, this knockout model is optimized for investigations into liver-specific oncogenic mechanisms, metabolic regulation, and stress adaptation.

Hep-G2 cells were established from a liver biopsy of a 15-year-old Caucasian male with hepatocellular carcinoma and are characterized by an adherent epithelial morphology. Widely used in drug metabolism, hepatotoxicity, and cancer research, these cells maintain many hepatic functions and express key regulatory proteins, including wild-type p53. This clinically derived background offers a relevant platform for evaluating SIRT7 function within transformed hepatocytes, particularly in the context of hepatocellular carcinoma progression and liver-specific metabolic pathways.

SIRT7 encodes an NAD+-dependent deacetylase that localizes to the nucleolus, where it deacetylates histone H3K18 to promote ribosomal RNA transcription by RNA polymerase I. Additionally, it deacetylates p53, attenuating its transcriptional activity, and modifies NME1 to reduce metastasis. SIRT7 is regulated by nutrient deprivation, oxidative stress, and DNA damage via AMPK, FOXO3, and p53. It interacts with RNA polymerase I subunits, U3 snoRNP components, and NPM1, linking metabolic signals to ribosome biogenesis and genomic stability. Key pathways influenced include rRNA processing, SIRT1 signaling, and p53-mediated senescence.

In hepatocellular carcinoma, SIRT7 overexpression correlates with aggressive phenotypes, and its disruption impairs proliferation and ribosome biogenesis. This knockout line enables exploration of SIRT7’s role in hepatocarcinogenesis, metabolic reprogramming, and senescence. With wild-type p53 in Hep-G2 cells, the model permits discrimination of p53-dependent and -independent effects of SIRT7 loss, including studies of nucleolar function and rRNA synthesis. It also supports analysis of DNA repair and stress survival mechanisms in liver cancer.

This knockout cell line enables a broad spectrum of experimental approaches, including studies of ribosome biogenesis, hepatocellular carcinoma progression, cellular senescence, and DNA damage responses. Representative techniques include western blotting for protein analysis, RT-qPCR for transcript quantification, ChIP-qPCR to assess histone H3K18 acetylation, immunofluorescence for subcellular localization, and co-immunoprecipitation for protein interaction mapping. Functional assays measuring proliferation, apoptosis, and migration/invasion, along with metabolic profiling, further elucidate SIRT7’s role in cancer cell behavior. For additional technical information, please contact Ascent Research.