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Cat. No. ARG31972

C12orf43 Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

The C12orf43 Knockout A-549 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout population of the A-549 human lung adenocarcinoma cell line. C12orf43 is an uncharacterized open reading frame, and its knockout in these cells provides a platform to explore its potential involvement in cell growth, survival, and epithelial?Cmesenchymal transition within a clinically relevant NSCLC model. Applications include cell viability and colony formation assays to assess proliferative and clonogenic capacity, transwell migration and invasion studies to evaluate metastatic behavior, and molecular analyses via western blotting and RT-qPCR. This cell pool is ideal for functional genomics and drug target validation in lung adenocarcinoma research.

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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

    C12orf43

    Gene Identifier

    NCBI Gene ID 64897

    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 C12orf43 Knockout A-549 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human A-549 lung adenocarcinoma cell line. In this product, the C12orf43 gene has been targeted for disruption using CRISPR/Cas9, yielding a heterogeneous mixture of cells with variable indel profiles at the target locus. This polyclonal format provides a robust loss-of-function system that avoids the biases of single-cell cloning, offering a population-averaged view of gene function. The edited cells are supplied as a ready-to-use pool, facilitating immediate functional assays without the need for further clonal isolation.

The A-549 cell line, established from the alveolar basal epithelium of a 58-year-old male NSCLC patient, is a quintessential model for lung adenocarcinoma research. These adherent epithelial cells harbor clinically relevant mutations, including KRAS G12S and TP53, and have been instrumental in elucidating mechanisms of tumorigenesis and therapeutic resistance. Their robust growth characteristics and compatibility with standard molecular biology techniques make them a preferred host for gene-editing studies.

C12orf43 remains an uncharacterized open reading frame with no validated upstream regulators, downstream effectors, or interacting proteins. Its molecular function is currently undefined, and it has not been assigned to any canonical signaling cascade. However, context-dependent hints suggest possible involvement in cell proliferation, survival, and epithelial?Cmesenchymal transition. The complete absence of functional annotation makes the C12orf43 knockout model a powerful starting point for discovery biology aimed at uncovering new regulatory nodes.

Given the clinical relevance of A-549 cells as a model for lung adenocarcinoma, C12orf43 knockout in this background enables direct investigation of the gene??s role in tumor cell growth, survival, and invasive capacity. The polyclonal editing ensures that functional outcomes reflect the average behavior of the edited population, minimizing clonal outliers. This model is well-suited for unbiased screens to uncover vulnerabilities associated with poorly annotated genes in NSCLC. Furthermore, the epithelial origin of A-549 cells supports studies of EMT-linked processes, a key determinant of metastatic dissemination.

Key applications include cell viability and colony formation assays to measure proliferative and clonogenic potential, transwell migration and invasion assays to assess metastatic behavior, and western blotting and RT-qPCR for protein and mRNA expression analysis. These cells can be employed in synthetic lethality screens, three-dimensional culture models, and target validation studies in drug discovery pipelines. The C12orf43 Knockout A-549 Polyclonal Cells serve as a flexible platform for both academic and industrial researchers focused on decoding the functions of orphan genes in lung adenocarcinoma. For further information, please contact Ascent Research.

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