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. 2020 Apr 29;9(4):42. doi: 10.1038/s41389-020-0226-z

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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 Immunofluorescence was conducted to visualize the expression of c-Myc in Huh7 cells with ACSL4 knockdown (c-Myc in green; DAPI in blue; scale bar: 50 μm). b Endogenous c-Myc protein levels following transfection (24 h) of 500 and 1000 ng of plasmid expressing pcDNA-ACSL4 in Bel-7402 and PLC/PRF5 cells. c qRT-PCR analysis of c-Myc in ACSL4 knockdown or overexpressed HCC cell lines. GAPDH was selected as the internal control. Data are presented as the mean ± SD (n = 3 biological replicates). The data were analyzed using Student’s t-test. NS: not significant. d Effect of protein synthesis inhibitor cycloheximide (CHX, 10 μg/ml) on c-Myc stability in ACSL4-depleted Huh7 cells and ACSL4 overexpressed PLC/PRF5 cells in a time course. The protein expression of ACSL4 and c-Myc was analyzed by western blotting (left) and semi-quantification (right). GAPDH was used as an internal standard.