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Cat. No. ARG31833

KHNYN Knockout NCI-H1975 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Carcinoma

The KHNYN Knockout NCI-H1975 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of NCI-H1975 lung adenocarcinoma cells, with targeted disruption of the KHNYN gene. KHNYN encodes a putative RNA-binding endoribonuclease implicated in mRNA processing, miRNA biogenesis, and RNA degradation, interacting with DICER1 and AGO2. This model enables functional studies of post-transcriptional regulation in EGFR-mutant NSCLC and drug resistance. Applications include transcriptomic profiling (RNA-seq), target validation (RT-qPCR, western blotting), and functional assays (cell proliferation, apoptosis, drug sensitivity with osimertinib).

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    NCI-H1975

    Sex of Donor

    Female

    Gene Name

    KHNYN

    Gene Identifier

    NCBI Gene ID 23351

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    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 KHNYN Knockout NCI-H1975 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of the human lung adenocarcinoma cell line NCI-H1975, engineered to disrupt the KHNYN gene. This polyclonal knockout product provides a heterogeneous pool of cells with targeted gene disruption, suitable for functional studies of KHNYN in RNA biology and cancer. Researchers can utilize this model to examine the consequences of KHNYN loss on transcriptome dynamics without the limitations of single-cell clone selection.

The host cell line, NCI-H1975, is a widely used non-small cell lung cancer (NSCLC) model derived from a female patient with lung adenocarcinoma. These cells harbor activating EGFR L858R and T790M mutations, rendering them dependent on EGFR signaling and resistant to first-generation tyrosine kinase inhibitors. The NCI-H1975 background is particularly relevant for investigating mechanisms of acquired drug resistance and for testing targeted therapies against mutant EGFR.

KHNYN encodes a putative RNA-binding protein with endoribonuclease activity, involved in mRNA processing and stability. It likely participates in RNA degradation and miRNA biogenesis, interacting with RNA molecules and possibly components of the RNA exosome. Representative pathway components linked to KHNYN include DICER1 and AGO2, key factors in miRNA maturation and function. Mechanistically, KHNYN influences post-transcriptional regulation by cleaving or processing RNA targets, thereby modulating mRNA and miRNA expression. Its disruption may dysregulate oncogenic signaling networks in NSCLC cells.

In the context of NCI-H1975 cells, KHNYN knockout provides a powerful tool to dissect how RNA regulatory pathways contribute to lung adenocarcinoma progression and drug resistance. Given the EGFR mutation background, this model enables investigation of interactions between oncogenic kinase signaling and post-transcriptional gene regulation. Researchers can explore whether KHNYN loss sensitizes cells to osimertinib or other EGFR inhibitors, or whether it impacts epithelial-mesenchymal transition and metastatic potential.

Typical applications include RNA sequencing to map transcriptomic changes, RT-qPCR validation of candidate mRNA and miRNA targets, and western blotting to assess EGFR pathway activity. Cell proliferation, apoptosis, and drug sensitivity assays (e.g., osimertinib) are used to evaluate functional consequences of KHNYN disruption. This model supports screening for novel RNA regulators in NSCLC drug resistance. For further information or customized requests, please contact Ascent Research.

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