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Cat. No. ARG32369

BIN3 Knockout SK-HEP-1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Liver

  • Disease:

    Adenocarcinoma

Ascent Research??s BIN3 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of human liver adenocarcinoma cells with targeted disruption of the BIN3 gene. BIN3 encodes a BAR domain adapter that regulates integrin internalization and signaling via interactions with ITGB1 and FAK, influencing cell adhesion, migration, and autophagy. This knockout model is ideal for studying BIN3??s role in hepatocellular carcinoma metastasis, integrin trafficking, and autophagy, as well as for screening anti-metastatic drugs. Standard assays including Western blot, Transwell migration, and immunofluorescence are readily applicable.

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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

    BIN3

    Gene Identifier

    NCBI Gene ID 55909

    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 BIN3 Knockout SK-HEP-1 Polyclonal Cells product from Ascent Research provides a CRISPR/Cas9-mediated gene-disrupted cell population targeting BIN3 in the human SK-HEP-1 liver adenocarcinoma cell line. This polyclonal knockout pool is designed to enable loss-of-function studies without clonal isolation, offering a heterogeneous population representative of diverse editing events. The product facilitates robust investigation of BIN3-dependent cellular processes in a cancer-relevant context.

SK-HEP-1 is a widely used hepatocellular carcinoma cell line originally derived from the ascitic fluid of a 52-year-old male patient with liver adenocarcinoma. The cells exhibit a mixed phenotype with both endothelial and epithelial characteristics, making them particularly valuable for studies of tumor cell plasticity, metastasis, and angiogenesis. Their adherent growth and reproducible behavior in standard culture conditions support a broad range of functional assays.

BIN3 encodes a BAR domain-containing adapter protein that plays a critical role in integrin internalization, endocytosis, and autophagy. Mechanistically, BIN3 interacts with integrin beta subunits such as ITGB1 and ITGB3, as well as ARF GTPases, dynamin, BIN1, and AMPH. Upstream signals from integrins (ITGA5/ITGB1), growth factors including EGF and HGF, and Rho GTPases (Rac1, Cdc42) converge on BIN3 to regulate focal adhesion dynamics. Downstream, BIN3 modulates key effectors including FAK (PTK2), Src kinase, actin polymerization, and autophagosome formation, thereby controlling cell adhesion, migration, and degradation pathways.

In SK-HEP-1 cells, loss of BIN3 function disrupts integrin recycling and attenuates FAK/Src signaling, leading to altered focal adhesion turnover and reduced cell motility. This perturbation is expected to impact hepatocellular carcinoma cell invasion and metastatic potential, making the knockout model highly relevant for studying tumor progression mechanisms. Additionally, BIN3??s role in autophagy may be interrogated in this context, providing insights into how cancer cells balance survival and death signals.

Researchers can employ this polyclonal BIN3 knockout SK-HEP-1 model in a variety of applications, including investigation of integrin trafficking dynamics, screening for anti-metastatic compounds, and elucidation of autophagy regulation in liver cancer. Representative assays that can be performed with these cells include Western blotting for BIN3, ITGB1, total and phosphorylated FAK; immunofluorescence to assess integrin localization; Transwell migration and invasion assays; cell adhesion assays; co-immunoprecipitation to probe BIN3?Cintegrin interactions; flow cytometry to measure integrin surface levels; and transcriptomic analysis by RNA-seq. For further information or to request a quote, please contact Ascent Research.

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