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Cat. No. ARG32481

GOLPH3 Knockout SK-HEP-1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Liver

  • Disease:

    Adenocarcinoma

The GOLPH3 Knockout SK-HEP-1 Polyclonal Cells represent a heterogeneous population of SK-HEP-1 human hepatic adenocarcinoma cells engineered with CRISPR/Cas9 to disrupt the GOLPH3 gene, providing a robust tool for functional genomics. Encoding a Golgi phosphoprotein that integrates AKT and mTOR signaling with vesicle trafficking, GOLPH3 is a key oncogenic driver in hepatocellular carcinoma and other cancers. Researchers can utilize these polyclonal knockout cells to explore tumorigenesis, drug resistance, and migration, employing techniques such as western blotting, immunofluorescence, and proliferation 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

    GOLPH3

    Gene Identifier

    NCBI Gene ID 64083

    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 GOLPH3 Knockout SK-HEP-1 Polyclonal Cells consist of a polyclonal population of SK-HEP-1 human hepatic adenocarcinoma cells engineered with CRISPR/Cas9-mediated disruption of the GOLPH3 gene. In contrast to monoclonal isolates, the polyclonal composition captures a broader spectrum of knockout-induced phenotypic variation, enhancing the robustness of functional studies. This knockout model provides a loss-of-function system to study GOLPH3-dependent cellular processes, eliminating potential clonal bias through a heterogeneous pool.

The SK-HEP-1 cell line, derived from the ascites of a patient with liver adenocarcinoma, is a well-established model for hepatocellular carcinoma (HCC). These epithelial-like cells retain key characteristics of hepatic tumor cells, including anchorage-independent growth and tumorigenicity in vivo, and are extensively utilized to explore hepatocarcinogenesis, drug sensitivity, and metastatic mechanisms, making them an ideal platform for GOLPH3 knockout analysis.

GOLPH3 encodes a Golgi-associated phosphoprotein central to vesicle trafficking, Golgi architecture, and secretion. It functions downstream of PI3K/AKT signaling, activated by AKT kinase-mediated phosphorylation. GOLPH3 interacts with MYO18A to form a complex that tethers Golgi membranes to the actin cytoskeleton, facilitating Golgi dispersal. It also binds DNA-PK, influencing the DNA damage response, and promotes mTOR activation via the AKT-mTOR axis, coupling growth signals to anabolic metabolism and cell survival.

In hepatocellular carcinoma, GOLPH3 overexpression drives oncogenic signaling, enhancing mTOR activity, proliferation, and resistance to therapeutics. Disrupting GOLPH3 in SK-HEP-1 cells allows dissection of its roles in HCC tumorigenesis, drug resistance, and cell migration. Loss of GOLPH3 may sensitize cells to DNA-damaging agents and mTOR inhibitors, providing a platform to study therapeutic vulnerabilities. Beyond liver cancer, this model is relevant to breast, lung, and prostate malignancies where GOLPH3 contributes to tumor progression.

Applications include investigating Golgi biology, signal transduction, and tumor cell behavior using assays such as western blotting, immunofluorescence, proliferation, migration, colony formation, and drug sensitivity testing. These polyclonal knockout cells are suited for functional genomics, target validation, and mechanistic studies. For additional information, validation data, or pricing, please contact Ascent Research.

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