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Cat. No. ARG38810

DIS3L2 Knockout huh-7 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Liver

  • Disease:

    Hepatocellular carcinoma

The DIS3L2 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from a human hepatocellular carcinoma cell line, engineered for loss-of-function studies of the 3'-5' exoribonuclease DIS3L2. This enzyme degrades uridylated RNAs downstream of ZCCHC6/11, regulating microRNAs such as pre-let-7 and the miR-200 family. Ideal for investigating microRNA decay, RNA surveillance, and tumor suppression mechanisms, this knockout model enables RT-qPCR, RNA-seq, and uridylation assays. It supports Perlman syndrome research and evaluation of RNA-targeting therapies. Contact Ascent Research for more information.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    Huh-7

    Sex of Donor

    Male

    Age

    57 years

    Gene Name

    DIS3L2

    Gene Identifier

    NCBI Gene ID 129563

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    DMEM

    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 SK-HEP-1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population generated from the SK-HEP-1 human hepatocellular carcinoma cell line, in which the gene encoding DIS3L2 has been disrupted. This heterogeneous pool of cells harbors diverse loss-of-function mutations at the target locus, enabling robust loss-of-function studies without clonal isolation. The model is designed for investigating the roles of DIS3L2 in RNA metabolism within a liver cancer context.

SK-HEP-1 is a widely used hepatocellular carcinoma cell line originally established from the ascitic fluid of a male patient with liver adenocarcinoma. These cells serve as a standard in vitro system for studying hepatic tumorigenesis, drug responses, and molecular mechanisms underlying liver cancer. Their tumor-derived background provides a pathologically relevant environment for examining the tumor-suppressive functions of RNA surveillance factors.

DIS3L2 encodes a 3′-5′ exoribonuclease that selectively degrades RNAs bearing 3′-terminal oligouridine tails. This activity is directed by ZCCHC6 (TUT7) and ZCCHC11 (TUT4), terminal uridylyl transferases that uridylate pre-let-7 and miR-200 family microRNAs. The LIN28A/LIN28B proteins promote pre-let-7 uridylation, thereby channeling these transcripts toward DIS3L2-mediated decay. Thus, DIS3L2 functions as a key effector in microRNA biogenesis control and broader cytoplasmic RNA surveillance. Its loss leads to accumulation of uridylated RNAs, disrupting gene expression networks relevant to development and cancer.

In hepatocellular carcinoma, DIS3L2 has been implicated as a putative tumor suppressor, and its inactivation may foster oncogenic transformation. The SK-HEP-1 polyclonal knockout model allows dissection of how DIS3L2 loss impacts RNA metabolism and cellular phenotypes in a liver cancer milieu. Researchers can probe the interplay between RNA decay pathways and tumor cell behavior, including proliferation, apoptosis, and metastatic potential, using this disease-relevant platform.

Research applications include RT-qPCR quantification of pre-let-7 and miR-200 family members, RNA sequencing to identify DIS3L2 substrates, and cRT-PCR for uridylation detection. Western blotting validates DIS3L2 knockout, while RNA stability and functional assays probe consequences on proliferation and apoptosis. The polyclonal knockout cells are suited for Perlman syndrome studies, tumor suppression mechanisms, and development of RNA-targeted drugs. For further details or custom inquiries, contact Ascent Research.

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