Аннотация:Notch1 inhibition resulted in stemness (SOX2, OCT3/4, NES), EMT (TWIST1, HES1, SNAIL1), CSCs (CD133) markers, c-MYC expression decrease and CDH1 (E-cadherin) expression increase suggesting that Notch pathway is involved in EMT. Loss of Notch1 did not influence cell proliferation in vitro but reduced migration potential. It was confirmed that Notch signalling interruption leads to reduction of stemness features: decreased drug resistance (A549 but not HCT116), ability to form tumourispheres and tumourigenic potential in vivo. ABC-transporter activity in HCT116 could be upregulated by TAZ/YAP signalling pathway and not by Notch. Moreover, reduced Notch1 expression increased the minimum inoculum cell dose for xenograft formation. The xenograft vascularisation assay revealed that Notch1 inhibition is not necessary for neovascularizaton but it is essential for angiogenesis but in tumour.Conclusion The Notch signalling pathway is important for maintaining the CSCs population, stemness and migration so Notch1 could be considered as a potential therapeutic target in lung and colorectal cancer.