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Cat. No. ARG33667

HMMR Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

The HMMR Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the HMMR gene has been disrupted in the A-549 human lung adenocarcinoma cell line. HMMR codes for the hyaluronan receptor RHAMM, which activates downstream effectors such as ERK1/2, AKT, and FAK to coordinate cell migration, adhesion, and proliferation. This model is suited for investigating mechanisms of cancer cell motility, hyaluronan signaling, and metastasis, particularly in lung cancer research. Researchers can apply the cells in wound healing, Transwell invasion, and phospho-protein analyses to study how loss of RHAMM alters interactions with CD44 and integrins under chemotactic or growth factor stimulation.

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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

    HMMR

    Gene Identifier

    NCBI Gene ID 3161

    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 HMMR Knockout A-549 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population targeting the HMMR gene in the A-549 human lung epithelial carcinoma cell line. This polyclonal pool comprises a heterogeneous collection of cells with biallelic gene disruptions introduced across the population, offering a robust loss-of-function model without clonal selection. The product serves as a ready-to-use tool for studying HMMR-dependent biological processes, enabling researchers to interrogate gene function in a disease-relevant adenocarcinoma background.

The parental A-549 cell line originates from a 58-year-old Caucasian male with alveolar basal epithelial adenocarcinoma and is widely employed as a model for non-small cell lung cancer. These adherent cells retain key characteristics of lung adenocarcinoma, including expression of epithelial markers and responsiveness to growth factors such as EGF and TGFB, making them suitable for mechanistic studies of tumor cell signaling, migration, and proliferation.

HMMR encodes the receptor for hyaluronan-mediated motility (RHAMM), a multifunctional protein that binds hyaluronan in the extracellular matrix and transduces signals to intracellular pathways. Upon ligation, RHAMM interacts with CD44, integrins, and SRC kinases, and engages downstream effectors including ERK1/2, AKT, FAK, CDC42, and RHOA. This signaling network integrates cues from growth factors (EGF), cytokines, and mechanical stress to regulate focal adhesion dynamics, actin cytoskeleton reorganization, and cell cycle progression, ultimately promoting cell adhesion, migration, transformation, and survival.

In A-549 cells, HMMR is endogenously expressed, and its overexpression has been linked to enhanced metastatic behavior in lung adenocarcinoma. Disruption of HMMR in this polyclonal population provides a physiologically relevant context to dissect its contributions to oncogenic motility and hyaluronan-driven signaling. The model enables side-by-side comparisons with wild-type A-549 cells to evaluate changes in invasive potential, response to microenvironmental stimuli, and sensitivity to therapeutic agents targeting the hyaluronan?CRHAMM axis.

Researchers can employ this knockout cell population in diverse functional assays, including wound healing and Transwell migration/invasion experiments to quantitatively assess directional motility. Western blotting and immunofluorescence microscopy allow for monitoring of phosphorylated ERK1/2 and FAK, as well as actin cytoskeletal architecture, while qPCR confirms HMMR transcript ablation. Typical applications extend to drug testing for anti-metastatic compounds, RNAi rescue experiments, and co-culture studies exploring tumor?Cstroma interactions. For additional product information or experimental support, please contact Ascent Research.

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