Data on the inhibition of cell proliferation and invasion by the D2A-Ala peptide derived from the urokinase receptor
Federico Furlan,
Gabriele Eden,
Marco Archinti,
Ralitsa Arnaudova,
Giuseppina Andreotti,
Valentina Citro,
Maria Vittoria Cubellis,
Andrea Motta,
Bernard Degryse
Affiliations
Federico Furlan
Dept. of Molecular Biology and Functional Genomics, DIBIT, Università Vita-Salute San Raffaele, Via Olgettina 58, 20132 Milan, Italy
Gabriele Eden
IFOM, FIRC Institute of Molecular Oncology, Via Adamello 16, 20139 Milan, Italy
Marco Archinti
Dept. of Molecular Biology and Functional Genomics, DIBIT, Università Vita-Salute San Raffaele, Via Olgettina 58, 20132 Milan, Italy
Ralitsa Arnaudova
Dept. of Molecular Biology and Functional Genomics, DIBIT, Università Vita-Salute San Raffaele, Via Olgettina 58, 20132 Milan, Italy
Giuseppina Andreotti
Istituto di Chimica Biomolecolare, Consiglio Nazionale delle Ricerche, Via Campi Flegrei 34, 80078 Pozzuoli (Naples), Italy
Valentina Citro
Dipartimento di Biologia, Università Federico II, Naples, Italy
Maria Vittoria Cubellis
Dipartimento di Biologia, Università Federico II, Naples, Italy
Andrea Motta
Istituto di Chimica Biomolecolare, Consiglio Nazionale delle Ricerche, Via Campi Flegrei 34, 80078 Pozzuoli (Naples), Italy
Bernard Degryse
Dept. of Molecular Biology and Functional Genomics, DIBIT, Università Vita-Salute San Raffaele, Via Olgettina 58, 20132 Milan, Italy; Corresponding author. Present address: School of Health & Human Performance, Dublin City University, Glasnevin, Dublin 9, Ireland.
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. Keywords: Peptide, Urokinase receptor, Cell proliferation, Cell invasion
