Correction: Aspartate β-hydroxylase expression promotes a malignant pancreatic cellular phenotype

Abstract

[This corrects the article DOI: 10.18632/oncotarget.2840.].

Figure 5. The β-hydroxylase activity of ASPH is required for its transforming activity.

MIA PaCa2 cells were stably transfected with empty vector (EV), “wild type” (WT)-ASPH, or H⁶⁷⁵Q-ASPH mutant and the levels of expression were confirmed by Western blot. There is low-level endogenous ASPH in MIA PaCa2 cells as shown here and in Fig. 1. Effects of EV, WT-ASPH and H⁶⁷⁵Q-ASPH on (A) cell proliferation, (B) migration, (C) invasion, and (D) colony formation are significantly different. (E and F) represents a Western blot demonstrating WT-ASPH induced activation of Notch signaling as determined by increased levels of Notch1 ICN, JAG2, as well as increased expression of downstream responsive genes HES1, HEY1, EpCAM, CD44, c-Myc, MMP2/9, cyclin D3 and PCNA. In contrast, the mutant H⁶⁷⁵Q ASPH construct shows significantly reduced activated Notch1 ICN, JAG2, as well as HES1, HEY1, EpCAM, CD44, c-Myc, MMP2/9, cyclin D3 and PCNA. The results suggest that the β-hydroxylase activity of ASPH is essential for Notch signaling activation. ^* p<0.05; ^** p<0.01; ^*** p<0.001.

Figure 7. Effect of SMI MO-I-1100 on the PC phenotype induced by exogenous or endogenous high-level of WT-ASPH expression.

MIA PaCa2 cells stably transfected with empty vector or the “wild type” ASPH construct via lentiviral transfection depicted in Fig. 2. The inhibitory effects of MO-I-1100 on (A) proliferation, (B) migration, (C) invasion, and (d) colony formation of MIA PaCa2 cells were observed. There is a significant reduction in the expression of Notch1 ICN, JAG2, as well as downstream responsive genes HES1, HEY1, EpCAM, CD44, c-Myc, MMP2/9, cyclin D3 and PCNA induced by MO-I-1100 compared to the DMSO treatment (E and F). ^* p<0.05; ^** p<0.01; ^*** p<0.001.