Furlan Federico, Eden Gabriele, Archinti Marco, Arnaudova Ralitsa, Andreotti Giuseppina, Citro Valentina, Cubellis Maria Vittoria, Motta Andrea, Degryse Bernard
Dept. of Molecular Biology and Functional Genomics, DIBIT, Università Vita-Salute San Raffaele, Via Olgettina 58, 20132 Milan, Italy.
IFOM, FIRC Institute of Molecular Oncology, Via Adamello 16, 20139 Milan, Italy.
Data Brief. 2019 Jan 9;22:903-908. doi: 10.1016/j.dib.2019.01.009. eCollection 2019 Feb.
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.
本文所呈现的数据与我们发表的题为《源自尿激酶受体的D2A - Ala肽在体内外发挥抗肿瘤作用》(Furlan等人,2018年)的研究文章相关。这些数据进一步扩展了我们对D2A - Ala肽抑制作用的理解。使用多种浓度的D2A - Ala绘制的剂量反应曲线表明,该肽本身对大鼠平滑肌细胞(RSMC)的增殖没有影响。然而,D2A - Ala以剂量依赖的方式抑制表皮生长因子(EGF)诱导的RSMC增殖。长达七天的动力学研究表明,D2A - Ala肽完全阻断了EGF促进的RSMC增殖。此外,D2A - Ala肽抑制HT 1080细胞向RSMC的侵袭。