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Cat. No. ARG38790

DIS3L Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

The DIS3L Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited heterogeneous population with targeted disruption of the DIS3L gene in the metastatic gastric adenocarcinoma HGC-27 cell line. DIS3L encodes the catalytic exoribonuclease of the cytoplasmic RNA exosome, which interacts with EXOSC1-10, SKIV2L, and EXOSC10 to degrade mRNAs and regulate gene expression. Loss of DIS3L disrupts RNA surveillance, potentially stabilizing oncogenic and tumor-suppressor transcripts. This model enables the study of RNA metabolism in gastric cancer, supporting assays such as RNA-seq, qRT-PCR, proliferation, apoptosis, and migration/invasion. For additional information, please 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

    HeLa

    Sex of Donor

    Female

    Age

    31 years

    Gene Name

    DIS3L

    Gene Identifier

    NCBI Gene ID 115752

    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

DIS3L Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 human gastric adenocarcinoma cell line. This product features targeted disruption of the DIS3L gene, providing a loss-of-function model for studying the roles of the cytoplasmic exosome catalytic subunit. The polyclonal format represents a heterogeneous pool of edited cells, enabling robust population-level analyses without clonal selection bias and is suitable for transcriptomic and functional assays.

The HGC-27 parental cell line is an adherent epithelial model established from a lymph node metastasis of a gastric adenocarcinoma. It is widely utilized to investigate molecular mechanisms of gastric cancer progression, including proliferation, invasion, and metastasis. The cell line retains aggressive tumor features, making it a clinically relevant platform to assess the impact of DIS3L deletion on oncogenic phenotypes and RNA metabolism dysregulation.

DIS3L encodes the essential 3′-5′ exoribonuclease of the cytoplasmic RNA exosome, a macromolecular complex that processes and degrades diverse RNA species. DIS3L directly interacts with exosome core components EXOSC1-10 and cofactors SKIV2L and EXOSC10 to catalyze the removal of poly(A) tails and subsequent RNA decay. This activity is central to mRNA surveillance pathways, including nonsense-mediated decay, and regulates the stability of transcripts encoding oncoproteins and tumor suppressors, thereby modulating gene expression in response to cellular cues.

In HGC-27 cells, knockout of DIS3L disrupts cytoplasmic RNA turnover, leading to accumulation of normally short-lived mRNAs and potential rewiring of signaling networks. This perturbation offers a unique opportunity to explore how impaired RNA surveillance contributes to gastric adenocarcinoma cell behavior, including altered proliferation rates, apoptosis resistance, and enhanced metastatic capacity. The model may aid in identifying RNA substrates whose misregulation drives gastric cancer malignancy.

Researchers can employ this knockout product in RNA-seq and qRT-PCR experiments to identify stabilized transcripts, cell proliferation and apoptosis assays to measure functional outcomes, and migration/invasion assays to evaluate metastatic potential. Western blotting and co-immunoprecipitation can validate protein expression changes and interactions with exosome components. For additional information or to discuss custom applications, please contact Ascent Research.

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