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Cat. No. ARG32390

BRMS1L Knockout SK-HEP-1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Liver

  • Disease:

    Adenocarcinoma

BRMS1L Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human SK-HEP-1 hepatocellular carcinoma line. Disruption of the BRMS1L metastasis suppressor gene derepresses epithelial-mesenchymal transition (EMT) drivers such as Snail and Slug and upregulates matrix metalloproteinases MMP-2 and MMP-9, leading to enhanced invasive potential. This model is ideal for studying hepatocellular carcinoma metastasis, NF-??B and SIN3-HDAC complex signaling, and EMT regulation. Compatible with migration assays, Western blotting, RNA-seq, and drug response testing, it provides a versatile platform for cancer research. For orders, contact Ascent Research.

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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

    BRMS1L

    Gene Identifier

    NCBI Gene ID 84312

    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 BRMS1L Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human SK-HEP-1 hepatocellular carcinoma cell line. This product provides a heterogeneous pool of cells with targeted disruption of the BRMS1L gene, enabling loss-of-function studies in a liver cancer context. The polyclonal format preserves biological variability and is suitable for assays where a pure monoclonal knockout is not essential.

SK-HEP-1 cells were originally isolated from the ascites of a patient with liver adenocarcinoma and exhibit an epithelial morphology. This cell line is widely used as a model for hepatocellular carcinoma (HCC) due to its invasive and metastatic properties, making it a relevant system for investigating tumor progression and metastasis.

BRMS1L (Breast Cancer Metastasis Suppressor 1-Like) encodes a metastasis suppressor that functions as a core component of the SIN3-HDAC transcriptional repressor complex. Within this complex, BRMS1L interacts with SIN3A, HDAC1, HDAC2, and BRMS1 to mediate histone deacetylation and gene silencing. Its tumor-suppressive activity is primarily associated with inhibition of epithelial-mesenchymal transition (EMT) by repressing transcription of key EMT drivers such as Snail and Slug. Additionally, BRMS1L suppresses matrix metalloproteinases MMP-2 and MMP-9, thereby reducing extracellular matrix degradation and invasion. The protein also negatively regulates NF-??B signaling, a pathway that promotes pro-invasive and pro-survival gene expression. Loss of BRMS1L function in these polyclonal knockout cells derepresses these targets, leading to a more aggressive phenotype.

Knockout of BRMS1L in SK-HEP-1 cells generates a powerful model for dissecting the molecular mechanisms of hepatocellular carcinoma metastasis. SK-HEP-1 cells inherently possess invasive characteristics, and ablation of BRMS1L further amplifies migratory and invasive capacities. This engineered system allows researchers to study the interplay between the SIN3-HDAC complex and EMT regulators, as well as the consequences on downstream effectors like MMP-2, MMP-9, and NF-??B. The polyclonal nature of the knockout population mimics the genetic heterogeneity often observed in tumors, providing a more realistic platform for drug response testing and pathway analysis.

Typical applications of the BRMS1L Knockout SK-HEP-1 Polyclonal Cells include cancer metastasis research, invasion and migration assays, wound healing assays, EMT studies, and investigation of tumor suppressor gene function. These cells are compatible with a wide range of downstream assays such as Western blotting, RT-qPCR, RNA-seq, ChIP-qPCR, and immunofluorescence. They are particularly suited for evaluating the transcriptional regulation of EMT and matrix remodeling genes, as well as for screening compounds that may reverse the metastatic phenotype. For further technical details and ordering information, please contact Ascent Research.

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