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Cat. No. ARG38797

DIS3L2 Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

DIS3L2 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of the A2780 ovarian carcinoma epithelial cell line. These cells model loss of function of the DIS3L2 exoribonuclease, which degrades uridylated RNAs such as pre-let-7 miRNAs, with key upstream regulators TUT4 and TUT7. This knockout system is ideal for investigating RNA decay, miRNA biogenesis, and cancer biology. Applications include RNA stability assays, RT-qPCR for let-7 levels, and transcriptomic analyses to study DIS3L2-dependent gene regulation in an ovarian cancer context.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    A549

    Sex of Donor

    Male

    Age

    58 years

    Derived From Site

    Lung

    Gene Name

    DIS3L2

    Gene Identifier

    NCBI Gene ID 129563

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    MEM

    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 DIS3L2 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the A2780 human ovarian carcinoma epithelial line. These cells contain a heterogeneous pool of DIS3L2 gene disruptions, creating a robust loss-of-function model for studying RNA metabolism. As a polyclonal knockout pool, the product offers a representative sample of knockout-induced genetic variation, suitable for population-level analyses. The CRISPR/Cas9-mediated gene disruption yields a mixed genotype that effectively abolishes DIS3L2 protein expression across the culture.

The A2780 cell line is an established model of ovarian endometrioid adenocarcinoma, derived from an untreated patient. These epithelial cells retain key features of the original tumor and are widely used in cancer research for studies of tumorigenesis, drug response, and gene regulation. They provide a disease-relevant system for exploring the role of RNA decay in ovarian cancer biology.

DIS3L2 encodes an exoribonuclease that degrades uridylated RNAs, critical for mRNA surveillance and miRNA biogenesis. It is activated by terminal uridylyltransferases TUT4 (ZCCHC11) and TUT7 (ZCCHC6), which add uridine tails to target RNAs. LIN28A indirectly affects this by modulating let-7 uridylation. Key substrates include uridylated let-7 precursors, mRNAs, and ncRNAs. DIS3L2 thus forms a functional axis with TUT4 and TUT7 in the uridylation-mediated decay pathway, regulating gene expression post-transcriptionally. This pathway is crucial for normal RNA turnover and its disruption has implications in cancer.

In the A2780 context, loss of DIS3L2 disrupts uridylation-dependent RNA decay, potentially altering let-7 miRNA processing and mRNA stability. Given associations with Perlman syndrome and Wilms tumor, this model aids in dissecting DIS3L2??s tumor-suppressive roles and how RNA metabolism aberrations drive cancer. It is ideal for studying impacts on proliferation, apoptosis, and drug sensitivity in ovarian cancer.

These polyclonal knockout cells are suitable for miRNA processing studies, RNA decay mechanism investigations, and transcriptome-wide analyses. Key assays include RT?qPCR for let-7 levels to monitor miRNA processing, RNA stability assays to measure decay rates of uridylated transcripts, western blotting to validate DIS3L2 protein depletion, RNA?seq to identify global transcriptomic changes, and reporter assays for functional analysis of mRNA decay. For further details and ordering information, please contact Ascent Research.

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