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. 2020 Aug 28;12(16):16304–16325. doi: 10.18632/aging.103660

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Copyright © 2020 Li et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution (CC BY) 3.0 License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Upregulated HOXD-AS1 facilitated the viability, migration and invasion of CCA cells. (A) The expression of HOXD-AS1 in CCLP-1, QBC939, TFK-1, RBE cells and normal HIBEC. (B) CCK-8 proliferation curves were drawn to show the impact of HOXD-AS1 on cellular proliferation. (C) EdU assay was performed to detect the effect of HOXD-AS1 on cellular proliferation. (D) The effect of HOXD-AS1 on cell colonies was revealed by colony formation assays. (E) The wound closure of CCA cells was evaluated by wound healing assays. (F) Transwell assays displayed that migrating cells were decreased in si-HOXD-AS1 cells and increased in QBC939 cells transfected with HOXD-AS1 plasmid. (G) The invasive ability of CCA cells was confirmed by transwell assay. (H) EMT-related proteins including epithelial marker (E-cadherin) and mesenchymal markers (snail and vimentin) were measured via western blot. ^*P < 0.05, ^**P < 0.01, ^***P < 0.001.