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. 2021 May 31;21:287. doi: 10.1186/s12935-021-01991-z

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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. 6 — GOLT1B regulates the expression and membrane translation of PD-L2. a The correlation between GOLT1B and immuno-infiltrating cells in CRC from TIMER database. b Co-culture of HCT116 and Jurkat cell showed that GOLT1B overexpression in cancer cells could induce Jurkat cells apoptosis and c inhibit the IFN-γ level in Jurkat cell. d The correlation between PD-L2 and GOLT1B in CRC from GEPIA2 database. e GOLT1B knockdown or overexpression could decrease and increase PD-L2 level in CRC cells, respectively. f The cell membrane and cytoplasm separation experiment showed that GOLT1B could upregulate the PD-L2 level on the cell membrane. g The CO-IP experiment confirmed the interaction between GOLT1B and PD-L2