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Cat. No. ARG32745

KDM4B Knockout SK-HEP-1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Liver

  • Disease:

    Adenocarcinoma

The KDM4B Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human liver adenocarcinoma cell line SK-HEP-1. This model disrupts KDM4B, a histone lysine demethylase that removes repressive H3K9me3 marks, and is regulated by HIF1A, E2F1, and EGFR signaling. KDM4B knockout leads to H3K9me3 accumulation, silencing of oncogenic targets such as CCNA2 and MMP9, and suppression of proliferation and invasion. Ideal for hepatocellular carcinoma epigenetics, demethylase inhibitor studies, and chromatin analysis via ChIP-qPCR, western blot, and functional assays.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    SK-HEP-1

    Sex of Donor

    Male

    Age

    52 years

    Gene Name

    KDM4B

    Gene Identifier

    NCBI Gene ID 23030

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    MEM (with NEAA)

    Supplement(s)

    10% Fetal Bovine Serum, 1% Penicillin-Streptomycin Solution

    Temperature

    37°C

    Atmosphere

    5% CO₂

  • Quality Control

    Sterility testing

    The bacterial, yeast, and fungi are not detected in these cells by daily monitor.

    Mycoplasma testing

    Negative for mycoplasma through PCR analysis

  • 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 KDM4B Knockout SK-HEP-1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-HEP-1 human liver adenocarcinoma cell line. This polyclonal pool harbors a targeted disruption of the KDM4B gene, creating a loss-of-function model in a mixed cell population. By eliminating KDM4B expression, researchers can probe its role in chromatin regulation and hepatocellular carcinoma biology without the constraints of clonal selection.

SK-HEP-1 is an adherent epithelial cell line originally isolated from ascites of a patient with liver adenocarcinoma, serving as a well-characterized in vitro model for hepatocellular carcinoma (HCC) despite potential endothelial-like features. It is widely employed to study HCC pathogenesis, metastasis, and therapeutic responses, offering a relevant context for investigating KDM4B-driven epigenetic mechanisms in liver cancer.

KDM4B is a histone lysine demethylase that erases repressive H3K9me2/me3 and H3K36me2/me3 marks, acting as a transcriptional coactivator. It is regulated by HIF1A under hypoxia, E2F1, and EGFR signaling, and directly interacts with chromatin modulators such as HDAC1/2, Sin3A, and the NCoR/SMRT complex, engaging in cross-talk with PRC2. By demethylating H3K9me3 at promoters of CCNA2, CCNE1, and MMP9, KDM4B facilitates their expression, thereby driving cell cycle progression and invasion while maintaining pluripotency-associated gene networks.

In SK-HEP-1 cells, KDM4B knockout precipitates H3K9me3 accumulation, silencing oncogenic targets and suppressing proliferation and invasive capacity, as shown in growth and migration assays. This disrupts the hypoxia?CKDM4B?CMMP9 axis and attenuates androgen receptor-mediated transcription, underscoring KDM4B’s critical role in maintaining the malignant HCC phenotype. The model is thus invaluable for dissecting KDM4B-dependent oncogenic pathways and testing demethylase inhibitors.

Applications span chromatin immunoprecipitation (ChIP-qPCR) to assess histone modifications, RT-qPCR and western blotting for target gene and H3K9me3 levels, and functional assays including MTT/CCK-8 proliferation, Transwell migration/invasion, and flow cytometric cell cycle analysis. These cells support hepatocellular carcinoma epigenetics research, demethylase inhibitor validation, oncogene/tumor suppressor studies, and drug target discovery. For technical inquiries, please contact Ascent Research.

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