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. 2021 Dec 4;16:24. doi: 10.1186/s13062-021-00312-8

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — LOXL1-AS1 accelerates cell proliferation, migration and invasion but represses cell apoptosis in HCC. A The expression level of LOXL1-AS1 in HCC cell lines and normal cell line was tested by qRT-PCR. B The interference efficiency of sh-LOXL1-AS1 in HCCLM3 and SK-HEP-1 cells was detected via qRT-PCR. C Colony formation assay estimated cell proliferative capacity in response to transfection of sh/LOXL1-AS1 and sh/NC. D EdU assay measured cell proliferation before and after silencing LOXL1-AS1. E, F JC-1 assay and TUNEL assay were utilized to measure apoptosis of cells transfected with sh/LOXL1-AS1 and sh/NC. G, H Transwell assay detected cell migratory and invasive capacities when LOXL1-AS1 was knocked down. **P < 0.01