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Cat. No. ARG36655

ANLN Knockout SK-Hep-1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Liver

  • Disease:

    Adenocarcinoma

ANLN Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population in SK-HEP-1 hepatocellular carcinoma cells, disrupting the ANLN gene. ANLN encodes anillin, a scaffold for RhoA, septins, and myosin II essential for cytokinesis and actomyosin contractility. This heterogeneous population avoids clonal biases. Overexpression of ANLN in liver cancer drives proliferation and metastasis. These knockout cells enable studies of cytokinesis failure, polyploidy, and reduced migration/invasion, and screening for ANLN-dependent drug sensitivities. They support applications like Western blotting, immunofluorescence, and RhoA activation 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

    ANLN

    Gene Identifier

    NCBI Gene ID 54443

    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 ANLN Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human hepatocellular carcinoma cell line SK-HEP-1. This product features targeted disruption of the ANLN gene using CRISPR/Cas9 technology, generating a heterogeneous pool of knockout cells. The polyclonal format avoids clonal artifacts and enables robust phenotypic screening of ANLN-dependent pathways without the need for single-cell cloning.

The host cell line, SK-HEP-1, is a human hepatocellular carcinoma cell line with mesenchymal characteristics, commonly used as a model for liver cancer metastasis and epithelial-mesenchymal transition (EMT). These cells exhibit a metastatic phenotype and provide a clinically relevant context for studying tumor cell migration, invasion, and the molecular mechanisms driving hepatocellular carcinoma progression.

ANLN encodes anillin, an actin-binding protein essential for cytokinesis, actomyosin contractility, and cell migration. Anillin scaffolds the contractile ring by interacting with RhoA, septins (SEPT2, SEPT6, SEPT7), actin, and myosin II, stabilizing cleavage furrow ingression. Its activity is regulated by upstream factors including transcription factors E2F1, FOXM1, MYC, and kinases CDK1 and Plk1, as well as RhoA GTPase. Downstream, anillin interacts with ECT2, Rac1, and PI(4,5)P2, positioning it as a central node in RhoA signaling and actin cytoskeleton organization.

In hepatocellular carcinoma, ANLN overexpression promotes proliferation, migration, and invasion, and correlates with poor prognosis. The ANLN knockout SK-HEP-1 polyclonal cells thus provide a valuable tool to dissect anillin??s role in liver cancer. Disruption of ANLN in this mesenchymal-like line is expected to impair cytokinesis, leading to binucleation and polyploidy, while reducing metastatic potential. This model enables investigation of ANLN-dependent EMT processes and RhoA-driven cytoskeletal dynamics.

Applications include Western blotting and RT-qPCR for ANLN validation, immunofluorescence for cleavage furrow defects, and flow cytometry for polyploidy assessment. Functional assays such as Transwell migration/invasion, MTT proliferation, and RhoA activation assays can be performed. These cells are ideal for studying cytokinesis failure, cancer cell motility, and ANLN-dependent drug sensitivities. For further details, please contact Ascent Research.

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