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 / F. Furlan, G. Eden, M. Archinti, R. Arnaudova, G. Andreotti, V. Citro, M.V. Cubellis, A. Motta, B. Degryse. - In: DATA IN BRIEF. - ISSN 2352-3409. - 22(2019 Feb), pp. 903-908. [10.1016/j.dib.2019.01.009]
Data on the inhibition of cell proliferation and invasion by the D2A-Ala peptide derived from the urokinase receptor
V. Citro;
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.File | Dimensione | Formato | |
---|---|---|---|
1-s2.0-S2352340919300101-main.pdf
accesso aperto
Tipologia:
Publisher's version/PDF
Dimensione
362.89 kB
Formato
Adobe PDF
|
362.89 kB | Adobe PDF | Visualizza/Apri |
Pubblicazioni consigliate
I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.