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Development of a new flippase-dependent mouse model for red fluorescence-based isolation of KRAS-G12D oncogene-expressing tumor cells

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F25%3A00635731" target="_blank" >RIV/68378050:_____/25:00635731 - isvavai.cz</a>

  • Result on the web

    <a href="https://link.springer.com/article/10.1007/s11248-024-00429-2?utm_source=getftr&utm_medium=getftr&utm_campaign=getftr_pilot&getft_integrator=scopus" target="_blank" >https://link.springer.com/article/10.1007/s11248-024-00429-2?utm_source=getftr&utm_medium=getftr&utm_campaign=getftr_pilot&getft_integrator=scopus</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1007/s11248-024-00429-2" target="_blank" >10.1007/s11248-024-00429-2</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Development of a new flippase-dependent mouse model for red fluorescence-based isolation of KRAS-G12D oncogene-expressing tumor cells

  • Original language description

    Proto-oncogene KRAS, GTPase (KRAS) is one of the most intensively studied oncogenes in cancer research. Although several mouse models allow for regulated expression of mutant KRAS, selective isolation and analysis of transforming or tumor cells that produce the KRAS oncogene remains a challenge. In our study, we present a knock-in model of oncogenic variant KRASG12D that enables the ,,activation,, of KRASG12D expression together with production of red fluorescent protein tdTomato. Both proteins are expressed from the endogenous Kras locus after recombination of a transcriptional stop box in the genomic DNA by the enzyme flippase (Flp). We have demonstrated the functionality of the allele termed RedRas (abbreviated KrasRR) under in vitro conditions with mouse embryonic fibroblasts and organoids and in vivo in the lung and colon epithelium. After recombination with adenoviral vectors carrying the Flp gene, the KrasRR allele itself triggers formation of lung adenomas. In the colon epithelium, it causes the progression of adenomas that are triggered by the loss of tumor suppressor adenomatous polyposis coli (APC). Importantly, cells in which recombination has successfully occurred can be visualized and isolated using the fluorescence emitted by tdTomato. Furthermore, we show that KRASG12D production enables intestinal organoid growth independent of epidermal growth factor (EGF) signaling and that the KRASG12D function is effectively suppressed by specific inhibitor MRTX1133.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30204 - Oncology

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2025

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Transgenic Research

  • ISSN

    0962-8819

  • e-ISSN

    1573-9368

  • Volume of the periodical

    34

  • Issue of the periodical within the volume

    1

  • Country of publishing house

    NL - THE KINGDOM OF THE NETHERLANDS

  • Number of pages

    19

  • Pages from-to

    9

  • UT code for WoS article

    001393523100004

  • EID of the result in the Scopus database

    2-s2.0-85214865148