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. 2020 Nov 9;11(11):961. doi: 10.1038/s41419-020-03158-6

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© The Author(s) 2020

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — a, b Protein level of CD44s, caspase-1, and NLRP3 in five HCC cell lines were detected by western blot. The ratio of CD44s/GAPDH and caspase-1/CD44s was analyzed for the correlation. c Q-PCR analysis was performed to measure the mRNA expression of CASP1, NLRP3, and IL1B in control (siCon group) or CD44s deficient cells (siCD44 group). d, e Immunoblot analysis indicated that the caspase-1/IL1B pathway was inactivated in siCD44 cells. P10 refers to the active form of caspase-1. Cleaved IL1B refers to the mature form of IL1B. f Caspase-1 activity analysis showed CD44s knockdown inactivated caspase-1 capacity. Data are means ± SEM from 3 independent experiments, * means p < 0.05, ** means p < 0.01, *** means p < 0.001 by unpaired student t test.