Supplementary Material for:

Squalene epoxidase drives NAFLD-induced hepatocellular carcinoma and is a pharmaceutical target

Dabin Liu, Chi Chun Wong, Li Fu, Huarong Chen, Liuyang Zhao, Chuangen Li, Yunfei Zhou, Yanquan Zhang, Weiqi Xu, Yidong Yang, Bin Wu, Gong Cheng, Paul Bo-San Lai, Nathalie Wong, Joseph J. Y. Sung, Jun Yu*

*Corresponding author. Email: junyu{at}cuhk.edu.hk

Published 18 April 2018, Sci. Transl. Med. 10, eaap9840 (2018)
DOI: 10.1126/scitranslmed.aap9840

This PDF file includes:

• Fig. S1. SQLE expression in NAFLD-HCC is controlled by transcription factors.
• Fig. S2. Transcription factors SREBP2 and MEIS1 bind to SQLE promoter region and activate SQLE gene expression.
• Fig. S3. SQLE promotes HCC cell growth.
• Fig. S4. SQLE in HCC cell lines promoted cell cycle progression at G₁-S phase and inhibited apoptosis induction.
• Fig. S5. Sqle tg expression in mice induced apoptosis and the expression of proinflammatory cytokines and chemokines.
• Fig. S6. Cholesteryl ester and cholesterol concentrations are increased in NAFLD-HCC.
• Fig. S7. Oncogenic function of SQLE is dependent on the PTEN/PI3K/AKT/mTOR pathway.
• Fig. S8. SQLE silences PTEN expression through ROS-mediated DNA hypermethylation.
• Fig. S9. SQLE inhibitor terbinafine suppressed NAFLD-HCC growth in vitro and in vivo.
• Table S1. Epigenetic Chromatin Modification Enzymes PCR Array data.
• Table S2. Hypermethylated genes in LO2-SQLE cells.
• Table S3. Hypomethylated genes in LO2-SQLE cells.
• Table S4. Clinicopathological features of SQLE mRNA expression in our HCC cohort.
• Table S5. Clinicopathological features of SQLE mRNA expression in TCGA HCC cohort.
• Table S6. Primers used in this study.
• Table S7. Antibodies used in this study.

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