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Cat. No. ARG37335

BICC1 Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

The BICC1 Knockout HeLa Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal population of HeLa cervical adenocarcinoma cells with loss-of-function of the BICC1 RNA-binding protein. BICC1 negatively regulates Wnt/??-catenin signaling by suppressing DVL2 and PKD1 translation; its disruption leads to pathway hyperactivation and altered cell migration and polarity. This model is ideal for cancer biology, Wnt signaling, and cell migration research. Key applications include reporter assays, Western blotting for DVL2, PKD1, and ??-catenin, and functional migration/invasion assays. 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

    HeLa

    Sex of Donor

    Female

    Age

    31 years

    Gene Name

    BICC1

    Gene Identifier

    NCBI Gene ID 80114

    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 BICC1 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa cell line, providing a loss-of-function model for the BICC1 gene. This heterogeneous pool contains a mixture of cells with various editing events, enabling population-level analysis of BICC1 disruption. It serves as a robust tool for studying BICC1??s role in Wnt/??-catenin signaling regulation and cell migration without the influence of clonal artifacts.

HeLa cells are a human cervical adenocarcinoma epithelial cell line widely employed in biomedical research. Their well-characterized signaling networks, rapid proliferation, and relevance to cancer biology make them an ideal host for investigating BICC1 function. The cells exhibit active Wnt signaling and migratory properties, aligning with the pathway of interest.

BICC1 encodes an RNA-binding protein that negatively regulates Wnt/??-catenin signaling by controlling the translation of downstream targets. Under normal conditions, BICC1 suppresses DVL2 and PKD1 protein levels, thereby attenuating ??-catenin stabilization and transcriptional activity. The miR-17~92 cluster upstream represses BICC1 expression, forming a regulatory loop. Knockout of BICC1 lifts this translational control, leading to upregulation of DVL2 and PKD1 and subsequent hyperactivation of Wnt/??-catenin signaling via the Frizzled?CDVL2?CGSK3?¨C??-catenin axis. This dysregulation impacts planar cell polarity and cell migration programs.

In the HeLa context, BICC1 knockout offers a relevant model for cervical adenocarcinoma research, where Wnt pathway aberrations frequently occur. The polyclonal nature avoids single-clone bias, permitting robust assessment of BICC1??s impact on tumor cell migration and polarity. Furthermore, shared pathway components with ADPKD, including PKD1, extend the model??s utility to renal cystogenesis studies.

Researchers can employ this knockout model in Wnt/??-catenin luciferase reporter assays, Western blotting for DVL2, PKD1, and ??-catenin, and RT-qPCR for downstream targets like Axin2 and Cyclin D1. Migration and invasion assays quantify functional outcomes, while immunofluorescence for polarity markers reveals cellular asymmetry defects. Additional applications in cancer biology and kidney disease modeling are readily supported. For further inquiries, please contact Ascent Research.

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