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. 2020 Nov 27;10:139. doi: 10.1186/s13578-020-00499-9

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© The Author(s) 2020

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. 3 — KLHL18 regulates non-small cell lung cancer cell proliferation, migration, and invasion through the PI3K/AKT/mTOR pathway. a Spectrometry analysis with NCI-A549 cells revealed that KLHL18 protein can bind to PI3KP85α. b, c The effect of KLHL18 protein expression on the expression of effector proteins and pathway proteins in the b NCI-A549 and c NCI-H1299 cell lines. The lower graph corresponds to the gray value statistical graph, *P < 0.05, **P < 0.01. d, e PD-L1 protein levels decreased after a PI3K pathway inhibitor was added in both NCI-A549 (d) and NCI-H1299 (e) cell lines. The lower graph corresponds to the gray value statistical graph of various protein changes, *P < 0.05, **P < 0.01. f In the qRT-PCR experiments, the mRNA level of PI3KP85α did not change with the expression of KLHL18