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. 2017 Jun 22;38(2):785–798. doi: 10.3892/or.2017.5742

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Copyright: © Lang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 7. — linc-CCAT2 regulates HUVEC migration, proliferation, and tube formation in vitro. (A) The linc-CCAT2 expression levels were evaluated by qRT-PCR in linc-CCAT2 overexpression, downregulation, negative control, and normal HUVECs. linc-CCAT2 overexpression in HUVECs exhibited the highest expression level of linc-CCAT2, while downregulation of linc-CCAT2 in HUVECs exhibited the lowest expression level of linc-CCAT2. (B and C) The migration ability was assessed with the scratch-wound assay; linc-CCAT2 overexpression increased HUVEC migration, while downregulation of linc-CCAT2 significantly decreased HUVEC migration. (D) The proliferation was assessed with the CCK-8 assay; linc-CCAT2 overexpression promoted HUVEC proliferation, while linc-CCAT2 downexpression inhibited HUVEC proliferation. (E-H) The tube formation assay was performed on growth factor-reduced Matrigel. The total number of branching points, total tube length, and total loops at 6 h in the linc-CCAT2 overexpression in HUVECs was higher than in the negative control HUVECs, while downregulation of linc-CCAT2 in HUVECs was lower than the negative control HUVECs. (*P<0.05 when compared to the negative control; ^#P<0.05 when compared to the negative control). HUVECs, human umbilical vein endothelial cells; qRT-PCR, quantitative reverse-transcriptase polymerase chain reaction; CCK-8, Cell Counting Kit-8 assay.