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Multiphoton Microscopy Reveals DAPK1-Dependent Extracellular Matrix Remodeling in a Chorioallantoic Membrane (CAM) Model

Identifikátory výsledku

  • Kód výsledku v IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F22%3A00558228" target="_blank" >RIV/68378050:_____/22:00558228 - isvavai.cz</a>

  • Výsledek na webu

    <a href="https://www.mdpi.com/2072-6694/14/10/2364" target="_blank" >https://www.mdpi.com/2072-6694/14/10/2364</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.3390/cancers14102364" target="_blank" >10.3390/cancers14102364</a>

Alternativní jazyky

  • Jazyk výsledku

    angličtina

  • Název v původním jazyce

    Multiphoton Microscopy Reveals DAPK1-Dependent Extracellular Matrix Remodeling in a Chorioallantoic Membrane (CAM) Model

  • Popis výsledku v původním jazyce

    Simple Summary The formation of metastasis is not only intricately orchestrated by cancer cells but is also affected by the surrounding extracellular matrix (ECM). The barrier function of the ECM represents an obstacle that cancer cells have to overcome to disseminate from the primary tumor to form metastasis in distant organs. Here, we demonstrate an approach to studying the remodeling of a collagen-rich ECM by colorectal tumor cells using multiphoton microscopy (MPM). This approach allows the analysis of the invasion front of tumors grown on the CAM in 3D. MPM is superior to conventional histology, which is limited to 2D analysis and needs extensive tissue preparation. Cancer cells facilitate tumor growth by creating favorable tumor micro-environments (TME), altering homeostasis and immune response in the extracellular matrix (ECM) of surrounding tissue. A potential factor that contributes to TME generation and ECM remodeling is the cytoskeleton-associated human death-associated protein kinase 1 (DAPK1). Increased tumor cell motility and de-adhesion (thus, promoting metastasis), as well as upregulated plasminogen-signaling, are shown when functionally analyzing the DAPK1 ko-related proteome. However, the systematic investigation of how tumor cells actively modulate the ECM at the tissue level is experimentally challenging since animal models do not allow direct experimental access while artificial in vitro scaffolds cannot simulate the entire complexity of tissue systems. Here, we used the chorioallantoic membrane (CAM) assay as a natural, collagen-rich tissue model in combination with all-optical experimental access by multiphoton microscopy (MPM) to study the ECM remodeling potential of colorectal tumor cells with and without DAPK1 in situ and even in vivo. This approach demonstrates the suitability of the CAM assay in combination with multiphoton microscopy for studying collagen remodeling during tumor growth. Our results indicate the high ECM remodeling potential of DAPK1 ko tumor cells at the tissue level and support our findings from proteomics.

  • Název v anglickém jazyce

    Multiphoton Microscopy Reveals DAPK1-Dependent Extracellular Matrix Remodeling in a Chorioallantoic Membrane (CAM) Model

  • Popis výsledku anglicky

    Simple Summary The formation of metastasis is not only intricately orchestrated by cancer cells but is also affected by the surrounding extracellular matrix (ECM). The barrier function of the ECM represents an obstacle that cancer cells have to overcome to disseminate from the primary tumor to form metastasis in distant organs. Here, we demonstrate an approach to studying the remodeling of a collagen-rich ECM by colorectal tumor cells using multiphoton microscopy (MPM). This approach allows the analysis of the invasion front of tumors grown on the CAM in 3D. MPM is superior to conventional histology, which is limited to 2D analysis and needs extensive tissue preparation. Cancer cells facilitate tumor growth by creating favorable tumor micro-environments (TME), altering homeostasis and immune response in the extracellular matrix (ECM) of surrounding tissue. A potential factor that contributes to TME generation and ECM remodeling is the cytoskeleton-associated human death-associated protein kinase 1 (DAPK1). Increased tumor cell motility and de-adhesion (thus, promoting metastasis), as well as upregulated plasminogen-signaling, are shown when functionally analyzing the DAPK1 ko-related proteome. However, the systematic investigation of how tumor cells actively modulate the ECM at the tissue level is experimentally challenging since animal models do not allow direct experimental access while artificial in vitro scaffolds cannot simulate the entire complexity of tissue systems. Here, we used the chorioallantoic membrane (CAM) assay as a natural, collagen-rich tissue model in combination with all-optical experimental access by multiphoton microscopy (MPM) to study the ECM remodeling potential of colorectal tumor cells with and without DAPK1 in situ and even in vivo. This approach demonstrates the suitability of the CAM assay in combination with multiphoton microscopy for studying collagen remodeling during tumor growth. Our results indicate the high ECM remodeling potential of DAPK1 ko tumor cells at the tissue level and support our findings from proteomics.

Klasifikace

  • Druh

    J<sub>imp</sub> - Článek v periodiku v databázi Web of Science

  • CEP obor

  • OECD FORD obor

    10601 - Cell biology

Návaznosti výsledku

  • Projekt

    Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

  • Návaznosti

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Ostatní

  • Rok uplatnění

    2022

  • Kód důvěrnosti údajů

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

Údaje specifické pro druh výsledku

  • Název periodika

    Cancers (Basel)

  • ISSN

    2072-6694

  • e-ISSN

    2072-6694

  • Svazek periodika

    14

  • Číslo periodika v rámci svazku

    10

  • Stát vydavatele periodika

    CH - Švýcarská konfederace

  • Počet stran výsledku

    18

  • Strana od-do

    2364

  • Kód UT WoS článku

    000803172200001

  • EID výsledku v databázi Scopus