The data presented in this article are connected to our research article entitled "D2A-Ala peptide derived from the urokinase receptor exerts anti-tumoural effects in vitro and in vivo" (Furlan et al., 2018). These data further extend our understanding of the inhibitory effects of D2A-Ala peptide. Dose-response curve using a wide range of concentrations of D2A-Ala shows that this peptide has no effects per se on proliferation of rat smooth muscle cells (RSMC). However, D2A-Ala dose-dependently inhibits epidermal growth factor (EGF)-induced RSMC proliferation. Kinetics lasting up to seven days revealed that D2A-Ala peptide completely blocked EGF-promoted RSMC proliferation. Moreover, D2A-Ala peptide inhibited invasion of HT 1080 cells towards RSMC.

Data on the inhibition of cell proliferation and invasion by the D2A-Ala peptide derived from the urokinase receptor

Andreotti G;Motta A;
2019

Abstract

The data presented in this article are connected to our research article entitled "D2A-Ala peptide derived from the urokinase receptor exerts anti-tumoural effects in vitro and in vivo" (Furlan et al., 2018). These data further extend our understanding of the inhibitory effects of D2A-Ala peptide. Dose-response curve using a wide range of concentrations of D2A-Ala shows that this peptide has no effects per se on proliferation of rat smooth muscle cells (RSMC). However, D2A-Ala dose-dependently inhibits epidermal growth factor (EGF)-induced RSMC proliferation. Kinetics lasting up to seven days revealed that D2A-Ala peptide completely blocked EGF-promoted RSMC proliferation. Moreover, D2A-Ala peptide inhibited invasion of HT 1080 cells towards RSMC.
2019
Istituto di Chimica Biomolecolare - ICB - Sede Pozzuoli
Inglese
22
903
908
http://www.scopus.com/record/display.url?eid=2-s2.0-85060240607&origin=inward
Sì, ma tipo non specificato
peptide
urokinase recepto
cell proliferation
cell invasion
9
info:eu-repo/semantics/article
262
Furlan, F; Eden, G; Archinti, M; Arnaudova, R; Andreotti, G; Citro, V; Cubellis, Mv; Motta, A; Degryse, B
01 Contributo su Rivista::01.01 Articolo in rivista
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.14243/386010
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