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Cat. No. ARG37269

C17orf97 Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

This product is a polyclonal population of HeLa cells with CRISPR/Cas9-mediated knockout of the LIAT1 gene, which encodes a long intergenic non-coding RNA. LIAT1 acts as a ceRNA that sequesters miR-21 and miR-155, thereby modulating the expression of targets such as BCL2 and cyclin D1 to promote proliferation and survival. The HeLa host cell line is an HPV18-positive cervical adenocarcinoma model with inactivated p53 and pRb. This knockout tool enables functional studies of LIAT1 in cervical cancer, investigation of ceRNA mechanisms, and applications in assays including RT-qPCR, proliferation assays, and apoptosis analysis.

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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

    C17orf97

    Gene Identifier

    NCBI Gene ID 400566

    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 LIAT1 Knockout HeLa Polyclonal Cells product provides a heterogeneous population of HeLa cells with CRISPR/Cas9-mediated disruption of the LIAT1 gene, encoding a long intergenic non-coding RNA (lncRNA). This polyclonal knockout cell population serves as a robust loss-of-function model for investigating LIAT1 function without the biases associated with single-cell cloning.

The host HeLa cell line is derived from a human cervical adenocarcinoma and is positive for human papillomavirus type 18 (HPV18). The viral oncoproteins E6 and E7 inactivate the tumor suppressors p53 and pRb, respectively, endowing HeLa cells with an immortalized phenotype and making them a widely used model for HPV-related cervical cancer and general cell biology research.

LIAT1 acts as a competing endogenous RNA (ceRNA) that sponges specific microRNAs, including miR-21 and miR-155, thereby derepressing the expression of their mRNA targets such as BCL2 and CCND1. This mechanism promotes cell proliferation and survival by enhancing PI3K/AKT and MAPK/ERK signaling pathways, with downstream effectors including AKT, mTOR, and cyclin D1. LIAT1 is transcriptionally regulated by MYC, p53, and NF-??B, and it interacts with the PRC2 complex (via EZH2 and SUZ12) and the RNA-binding protein HuR, integrating epigenetic and post-transcriptional regulatory networks. Consequently, LIAT1 modulates apoptosis and cell cycle progression, directly impacting BAX/BCL2 balance and cyclin D1 expression.

In HeLa cells, LIAT1 contributes to oncogenic phenotypes by maintaining proliferation and resistance to apoptosis. Disruption of LIAT1 in this polyclonal knockout population is expected to attenuate these processes, providing a physiologically relevant context for studying lncRNA-mediated regulation in a cervical cancer background. The HPV-driven inactivation of p53 and pRb creates a unique environment where LIAT1??s ceRNA function may be particularly critical for sustaining malignant growth, making this knockout model valuable for dissecting lncRNA dependencies in HPV-associated malignancies.

This polyclonal knockout cell product is suited for a broad range of functional assays, including RT-qPCR and RNA-seq for transcriptomic profiling, ChIRP for lncRNA-chromatin interactions, dual-luciferase reporter assays for miRNA target validation, and phenotypic analyses such as MTT, colony formation, and flow cytometry-based apoptosis detection. By enabling loss-of-function studies, it supports research into the ceRNA hypothesis, lncRNA biology in cervical cancer, and the identification of therapeutic targets within lncRNA signaling networks. For additional details and ordering, please contact Ascent Research.

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