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- W3093094524 abstract "It is well known that neoplastic and stromal cells can affect each other during tumor progression. We have shown that carcinoma cells could induce myofibroblast-like differentiation of human primary normal mesenchymal stromal cells (HPNMSCs) via Notch1-dependent signaling and tumor suppressor P53 play an essential role in this process. This work was performed using cell lines: human lung carcinoma A549 (ATCC® CCL-185™), colorectal carcinoma lines HCT116 (ATCC® CCL-247™) and LIM1215 (ECACC General Collection 10092301), human fibrosarcoma HT1080 (ATCC® CCL-121™), hepatocellular carcinoma HEPG2 (ATCC® HB-8065™). We used lentiviral genetically engineered constructs to change target genes expression in HPNMSCs. Different in vitro assays (immunofluorescent analysis, FACS, RT-PCR, western-blotting, human mesenchymal stem cell functional identification kit, luciferase reporter activity, ELISA, molecular inhibitors, etc.) and nude mice assay were used for this study. Tumor cells activate Notch1-dependent signaling in HPNMSCs via direct contact interactions (Dll/Jagged-Notch1) upon co-cultivation if HPNMSCs express Notch1 with exposed extracellular domain. Such activation in HPNMSCs lead to P53-dependent increasing of α-smooth muscle actin (α-SMA) expression and myofibroblast-like phenotype acquisition. P53 plays a key role in this process as its inactivation prevented myofibroblast-like differentiation. Using γ-secretase inhibitor (DAPT) and luciferase CSL/RBP-reporter we have shown that P53 was necessary for α-SMA induction but not for initial activation of Notch1-dependent transcription. Transdifferentiated α-SMA-positive HPNMSCs were characterized by increased TGFb production and could stimulate tumor growth in nude mice. Notch1 silencing reduced tumor promotion properties of HPNMSCs and inhibited their differentiation. HPNMSCs tumor-stimulating potency depends on their ability to myofibroblast-like differentiation upon Notch signaling activation. Targeting key components of Notch signaling activation stages could partly interrupt tumor-stroma crosstalk and be promising for therapies." @default.
- W3093094524 created "2020-10-22" @default.
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- W3093094524 date "2020-10-01" @default.
- W3093094524 modified "2023-10-16" @default.
- W3093094524 title "64P Notch- and P53-dependent crosstalk between tumour and stromal cells" @default.
- W3093094524 doi "https://doi.org/10.1016/j.annonc.2020.08.2223" @default.
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