Quick Order Cart

Cat. No. ARG0401

SNHG17 Knockout Hep-G2 Cell Line

  • Product Type:

    Genome-edited Cells

  • Tissue Source:

    Liver

  • Disease:

    Hepatoblastoma

  • Gene Species:

    Homo sapiens (Human)

The SNHG17 Knockout Hep-G2 Cell Line offers a CRISPR/Cas9-edited loss-of-function model in human hepatocellular carcinoma cells. This product enables targeted disruption of the oncogenic lncRNA SNHG17, which promotes liver cancer through ceRNA-mediated regulation of miRNAs and downstream targets. SNHG17, activated by SP1, STAT3, and c-MYC, sponges miR-338-3p, miR-186-5p, and miR-485-5p to upregulate SOX4, ZEB1, and Cyclin D1, driving PI3K/AKT and Wnt/??-catenin signaling. The knockout cell line is ideal for proliferation, migration, invasion, and apoptosis assays, supporting research in ceRNA networks, drug target validation, and biomarker discovery.

Inquire Now

In stock

Ships next business day


Ask a Question

Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    Hep-G2

    Morphology

    Epithelial-like

    Age

    15 years

    Sex of Donor

    Male

    Gene Name

    SNHG17

    Gene Species

    Homo sapiens (Human)

    Gene Identifier

    NCBI Gene ID 388796

  • Culture Conditions

    Temperature

    37°C

    Atmosphere

    5% CO₂

  • Quality Control

    Sterility testing

    Daily monitoring confirms that the cells are free from bacterial, yeast, and fungal contamination.

    Mycoplasma testing

    Negative for mycoplasma through PCR analysis

    Pathogens

    Cells tested negative for HIV-1, HBV, and HCV.

  • Disclaimer

    Intended Use

    This product is intended for laboratory in vitro use only. lt is not intended for diagnostic, therapeutic, or clinical applications.

    Disclaimer

    Ascent Research endeavors to provide accurate and up-to-date product information. However, no warranties or representations are made regarding its completeness or reliability. References to scientific literature and patents are for informational purposes only, and the customer assumes sole responsibility for verifying their accuracy.

    By accepting this product, the customer acknowledges and agrees to assume all risks associated with its receipt, handling, storage, disposal, and use, including compliance with all applicable safety and environmental regulations and precautions. Relevant laws, regulations, and ethical guidelines must be followed in conducting any research, modifications, or derivatives derived from this product.

    This product is provided "AS IS", and except as expressly stated herein, Ascent Research disclaims all other warranties, express or implied. Under no circumstances shall Ascent Research, its affiliates, or representatives be liable for indirect, incidental, consequential, or punitive damages arising from the use of this material. While Ascent Research employs rigorous quality control measures, we shall not be held responsible for damages resulting from misidentification or misinterpretation of the provided materials.

Description

The SNHG17 Knockout Hep-G2 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from Homo sapiens hepatocellular carcinoma Hep-G2 cells. This loss-of-function model enables targeted disruption of the SNHG17 long non-coding RNA gene, providing a reliable system for investigating its roles in cancer. The cell line is maintained under standard culture conditions, ready for functional genomics and signaling studies.

The Hep-G2 host cell line originates from a liver biopsy of a 15-year-old male with hepatocellular carcinoma. These epithelial cells retain key hepatic functions, including drug metabolism and hepatotoxicity responses, making them a widely used model for liver biology. Hep-G2 cells express relevant cytochrome P450 enzymes and respond to genotoxic and metabolic stresses, offering a physiologically relevant context for studying hepatic carcinogenesis and compound safety.

SNHG17 functions as an oncogenic lncRNA that drives tumor cell proliferation, migration, and invasion primarily through a ceRNA mechanism. Upstream transcription factors SP1, STAT3, and c-MYC activate its expression. SNHG17 sponges tumor-suppressive miRNAs such as miR-338-3p, miR-186-5p, and miR-485-5p, thereby derepressing targets like SOX4, ZEB1, Cyclin D1, and Bcl-2. This network converges on PI3K/AKT and Wnt/??-catenin signaling, with representative components PIK3CA, AKT1, mTOR, CTNNB1, and TCF4, as well as EMT regulators CDH1, VIM, and SNAI1.

In Hep-G2 cells, SNHG17 knockout attenuates oncogenic signaling and allows dissection of lncRNA-mediated tumor progression. Loss of SNHG17 is anticipated to reduce PI3K/AKT and Wnt/??-catenin pathway activity, impair migration and invasion, and alter apoptosis and cell cycle profiles. This model facilitates validation of miRNA-lncRNA interactions and EMT regulation, and it can be used to evaluate whether Hep-G2 tumorigenicity depends on SNHG17.

The cell line supports multiple functional assays: MTT/CCK-8 proliferation, colony formation, wound healing, Transwell migration/invasion, flow cytometry for apoptosis and cell cycle, RT-qPCR, and Western blot for targets like Cyclin D1 and ZEB1. Dual luciferase reporter assays confirm miRNA interactions. Applications include lncRNA functional studies, ceRNA network investigation, drug target validation, and biomarker discovery in liver cancer. For further inquiries, contact Ascent Research.

Reset Password

    Reach Us Questions? Click Me Here!

    Fill out the form below and a member of our team will contact you shortly!

    *Required field



      Reach Us

      Fill out the form below and a member of our team will contact you shortly!

      *Required field

      Product Inquiry (Optional)