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Comment
. 2018 Jul 10;115(28):E6390-E6391.
doi: 10.1073/pnas.1808740115. Epub 2018 Jun 25.

Reply to Yoshida: Liver cancer stem cells: Identification and lipid metabolic reprogramming

Xian-Yang Qin  1 , Naoshi Dohmae  2 , Soichi Kojima  3
Affiliations
Comment

Reply to Yoshida: Liver cancer stem cells: Identification and lipid metabolic reprogramming

Xian-Yang Qin et al. Proc Natl Acad Sci U S A. .
No abstract available

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Fig. 1.
Fig. 1.
Proteomics characterization of EpCAM+ liver CSC-like cells. The EpCAM+/− cells were sorted from a HCC cell line JHH7 (1). Tryptic digests of whole-cell protein were analyzed by data-dependent nano-liquid chromatography–tandem mass spectrometry (nLC-MS/MS) (EASY-nLC and Q-Exactive; Thermo Scientific), and the obtained data were analyzed by Proteome Discoverer 2.2 (Thermo Scientific) using MASCOT program (Matrix Science). (A) Volcano plot of 4,110 proteins detected using nLC-MS/MS. The arrow indicates the increased EpCAM protein expression in EpCAM+ cells. (B) Top diseases’ or functions’ annotation associated with 123 differentially expressed proteins between EpCAM+/− cells (fold change more than 2 and adjusted P value less than 0.05) performed in Ingenuity Pathways Analysis platform. The pathways were ranked according to their activation z score, which can be used to predict either activated or inhibited state based on a statistically significant pattern match of up- and down-regulation, respectively. The pathways related with lipogenesis were highlighted in red. (C) Quantitative data of enzymes involved in FA synthesis including ACLY, ACACA, and FASN as well as desaturases including SCD1, FADS1, and FADS2 in EpCAM+/− cells detected using nLC-MS/MS. The mean averages from three biological replicates ± SD are shown.
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