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. 2020 Dec 2;11(12):1028. doi: 10.1038/s41419-020-03200-7

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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. 4 — a Western blot analysis showed that SKIL silencing decreased expression levels of autophagy markers (LC3, p62, and Beclin-1). b, c Immunofluorescence staining indicated significant decrease of autophagosome after SKIL silencing in both CALU-3 and NCI-H520 cell lines. Percentage of cells with LC3 vacuoles were counted and calculated from 100 cells in 20 fields d Western blot analysis showed that SKIL silencing decreased expression of TAZ and its downstream signaling factors (CTGF, CYR61). e, f Cycloheximide treatment resulted in faster TAZ protein degradation in SKIL-silenced CALU-3 (shSKIL) compared to control (shNC). g Co-immunoprecipitation assay showed that SKIL could bind to elements of Hippo complex (LATS2, Sav), but not TAZ. h Western blot analysis showed that overexpression of LATS2 led to increased phosphorylation of TAZ (p-TAZ) and decreased levels of TAZ. Further overexpression of SKIL reversed the effect of LATS2 overexpression on levels of p-TAZ and TAZ, without influencing LATS2 level. *P < 0.05, **P < 0.01. Experiments were performed in triplicate.