J Cancer 2021; 12(15):4661-4671. doi:10.7150/jca.53115

Research Paper

ApoM is an important potential protective factor in the pathogenesis of primary liver cancer

Yaping Bai1,2#, Wenjun Pei1#, Xiao Zhang3#, Huihao Zheng1, Changchun Hua1, Jiao Min1, Lisheng Hu1, Shuangqiu Du1,2, Zuyue Gong1, Jialin Gao1,4, Yao Zhang1,2✉

1. Anhui Province Key Laboratory of Biological Macro-molecules Research, Wannan Medical College, Wuhu 241002, China.
2. Department of Biochemistry and Molecular Biology, Wannan Medical Collage, Wuhu 241002, China.
3. Department of Pediatric Surgery, The First Affiliated Hospital Of USTC-Division of Life sciences and medicine, University of China, Hefei 230001, China.
4. Department of endocrine, The First Affiliated Hospital of Wannan Medical College, Wuhu 241002, China.
#These authors contributed equally to this work.

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Citation:
Bai Y, Pei W, Zhang X, Zheng H, Hua C, Min J, Hu L, Du S, Gong Z, Gao J, Zhang Y. ApoM is an important potential protective factor in the pathogenesis of primary liver cancer. J Cancer 2021; 12(15):4661-4671. doi:10.7150/jca.53115. Available from https://www.jcancer.org/v12p4661.htm

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Abstract

In recent years, abnormal liver lipid metabolism has emerged as one of the important pathogenesis pathways of primary liver cancer. It is highly important to identify the mechanisms to explore potential prevention and treatment targets. Apolipoprotein M is specifically expressed in the liver and participates in liver lipid metabolism, but the evidence that ApoM affects primary liver cancer is insufficient. The Cancer Genome Atlas (TCGA) database and clinical case analysis, as well as animal level and cell level analysis suggest that the expression level of ApoM gene in cancer tissues is lower than that in paracarcinoma tissues. Further experimental research found that the deletion of ApoM significantly increased the proliferation of mouse liver cancer cells (Hepa1-6) and inhibited the level of apoptosis induced by cisplatin. In addition, mouse liver cancer cells lacking ApoM showed stronger migration and invasion capabilities in transwell experiments. In contrast, overexpression of ApoM in Hepa1-6 cells and Huh-7 cells showed an inhibition of proliferation, up-regulation apoptosis and reduced migration and invasion. In vivo, the deletion of the ApoM accelerated tumorigenesis in nude mice and allowed the mice to develop liver tumor mutations more quickly under the induction of N-nitrosodiethylamine and the survival time of mice was shorter than that control. Therefore, ApoM may be a potential protective factor to inhibit the occurrence and development of primary liver cancer.

Keywords: apolipoprotein M, protective factor, primary liver cancer