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. 2023 Jul 3;13:124. doi: 10.1186/s13578-023-01060-0

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© The Author(s) 2023

Open Access This 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. 6 — PRSS56 overexpression promoted tumor progression in GC and CRC. (A) The GC and CRC cell lines stably overexpressing PRSS56 were constructed by lentivirus method. (B, C) The overexpression efficiency of PRSS56 in the relevant cell lines was measured by the qRT-PCR and western blotting assays. (D) Overexpression of PRSS56 promoted tumor cell proliferation in GC and CRC. (E, F) Overexpression of PRSS56 promoted tumor cell migration at indicated hours (24 and 48 h) in GC and CRC. (G, H) Overexpression of PRSS56 promoted tumor cell invasion in GC and CRC. **P < 0.01