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硬脂酸与棕榈酸的比例调节非B非C型肝癌细胞中的内质网应激和细胞凋亡。

Stearate-to-palmitate ratio modulates endoplasmic reticulum stress and cell apoptosis in non-B non-C hepatoma cells.

作者信息

Shibasaki Yasushi, Horikawa Makoto, Ikegami Koji, Kiuchi Ryota, Takeda Makoto, Hiraide Takanori, Morita Yoshifumi, Konno Hiroyuki, Takeuchi Hiroya, Setou Mitsutoshi, Sakaguchi Takanori

机构信息

Second Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan.

Department of Cellular & Molecular Anatomy, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan.

出版信息

Cancer Sci. 2018 Apr;109(4):1110-1120. doi: 10.1111/cas.13529. Epub 2018 Mar 6.

DOI:10.1111/cas.13529
PMID:29427339
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5891190/
Abstract

The increased prevalence of hepatocellular carcinoma (HCC) without viral infection, namely, NHCC, is a major public health issue worldwide. NHCC is frequently derived from non-alcoholic fatty liver (NAFL) and non-alcoholic steatohepatitis, which exhibit dysregulated fatty acid (FA) metabolism. This raises the possibility that NHCC evolves intracellular machineries to adapt to dysregulated FA metabolism. We herein aim to identify NHCC-specifically altered FA and key molecules to achieve the adaptation. To analyze FA, imaging mass spectrometry (IMS) was performed on 15 HCC specimens. The composition of saturated FA (SFA) in NHCC was altered from that in typical HCC. The stearate-to-palmitate ratio (SPR) was significantly increased in NHCC. Associated with the SPR increase, the ELOVL6 protein level was upregulated in NHCC. The knockdown of ELOVL6 reduced SPR, and enhanced endoplasmic reticulum stress, inducing apoptosis of Huh7 and HepG2 cells. In conclusion, NHCC appears to adapt to an FA-rich environment by modulating SPR through ELOVL6.

摘要

无病毒感染的肝细胞癌（HCC），即非病毒性肝细胞癌（NHCC）的患病率增加，是全球主要的公共卫生问题。NHCC通常源自非酒精性脂肪肝（NAFL）和非酒精性脂肪性肝炎，它们表现出脂肪酸（FA）代谢失调。这增加了NHCC进化细胞内机制以适应失调的FA代谢的可能性。我们在此旨在鉴定NHCC中特异性改变的FA和实现这种适应的关键分子。为了分析FA，对15个HCC标本进行了成像质谱（IMS）分析。NHCC中饱和脂肪酸（SFA）的组成与典型HCC中的不同。NHCC中硬脂酸与棕榈酸的比例（SPR）显著增加。与SPR增加相关，NHCC中ELOVL6蛋白水平上调。敲低ELOVL6可降低SPR，并增强内质网应激，诱导Huh7和HepG2细胞凋亡。总之，NHCC似乎通过ELOVL6调节SPR来适应富含FA的环境。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43b1/5891190/f6264d89b179/CAS-109-1110-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43b1/5891190/60829b52c395/CAS-109-1110-g002.jpg
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