Proteomics identifies new therapeutic targets of early-stage hepatocellular carcinoma
Hepatocellular carcinoma is the third leading cause of deaths from cancer worldwide. Infection with the hepatitis B virus is one of the leading risk factors for developing hepatocellular carcinoma, particularly in East Asia 1 . Although surgical treatment may be effective in the early stages, the fi...
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| Published in | Nature (London) Vol. 567; no. 7747; pp. 257 - 261 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
01.03.2019
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Hepatocellular carcinoma is the third leading cause of deaths from cancer worldwide. Infection with the hepatitis B virus is one of the leading risk factors for developing hepatocellular carcinoma, particularly in East Asia
1
. Although surgical treatment may be effective in the early stages, the five-year overall rate of survival after developing this cancer is only 50–70%
2
. Here, using proteomic and phospho-proteomic profiling, we characterize 110 paired tumour and non-tumour tissues of clinical early-stage hepatocellular carcinoma related to hepatitis B virus infection. Our quantitative proteomic data highlight heterogeneity in early-stage hepatocellular carcinoma: we used this to stratify the cohort into the subtypes S-I, S-II and S-III, each of which has a different clinical outcome. S-III, which is characterized by disrupted cholesterol homeostasis, is associated with the lowest overall rate of survival and the greatest risk of a poor prognosis after first-line surgery. The knockdown of sterol O-acyltransferase 1 (SOAT1)—high expression of which is a signature specific to the S-III subtype—alters the distribution of cellular cholesterol, and effectively suppresses the proliferation and migration of hepatocellular carcinoma. Finally, on the basis of a patient-derived tumour xenograft mouse model of hepatocellular carcinoma, we found that treatment with avasimibe, an inhibitor of SOAT1, markedly reduced the size of tumours that had high levels of SOAT1 expression. The proteomic stratification of early-stage hepatocellular carcinoma presented in this study provides insight into the tumour biology of this cancer, and suggests opportunities for personalized therapies that target it.
A subtype of early-stage hepatocellular carcinoma characterized by disrupted cholesterol homeostasis and associated with a poor prognosis responds to treatment with the SOAT1 inhibitor avasimibe in a patient-derived xenograft mouse model. |
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| AbstractList | Hepatocellular carcinoma is the third leading cause of deaths from cancer worldwide. Infection with the hepatitis B virus is one of the leading risk factors for developing hepatocellular carcinoma, particularly in East Asia1. Although surgical treatment may be effective in the early stages, the five-year overall rate of survival after developing this cancer is only 50-70%2. Here, using proteomic and phospho-proteomic profiling, we characterize 110 paired tumour and non-tumour tissues of clinical early-stage hepatocellular carcinoma related to hepatitis B virus infection. Our quantitative proteomic data highlight heterogeneity in early-stage hepatocellular carcinoma: we used this to stratify the cohort into the subtypes S-I, S-II and S-III, each of which has a different clinical outcome. S-III, which is characterized by disrupted cholesterol homeostasis, is associated with the lowest overall rate of survival and the greatest risk of a poor prognosis after first-line surgery. The knockdown of sterol O-acyltransferase 1 (SOAT1)-high expression of which is a signature specific to the S-III subtype-alters the distribution of cellular cholesterol, and effectively suppresses the proliferation and migration of hepatocellular carcinoma. Finally, on the basis of a patient-derived tumour xenograft mouse model of hepatocellular carcinoma, we found that treatment with avasimibe, an inhibitor of SOAT1, markedly reduced the size of tumours that had high levels of SOAT1 expression. The proteomic stratification of early-stage hepatocellular carcinoma presented in this study provides insight into the tumour biology of this cancer, and suggests opportunities for personalized therapies that target it. Hepatocellular carcinoma is the third leading cause of deaths from cancer worldwide. Infection with the hepatitis B virus is one of the leading risk factors for developing hepatocellular carcinoma, particularly in East Asia.sup.1. Although surgical treatment may be effective in the early stages, the five-year overall rate of survival after developing this cancer is only 50-70%.sup.2. Here, using proteomic and phospho-proteomic profiling, we characterize 110 paired tumour and non-tumour tissues of clinical early-stage hepatocellular carcinoma related to hepatitis B virus infection. Our quantitative proteomic data highlight heterogeneity in early-stage hepatocellular carcinoma: we used this to stratify the cohort into the subtypes S-I, S-II and S-III, each of which has a different clinical outcome. S-III, which is characterized by disrupted cholesterol homeostasis, is associated with the lowest overall rate of survival and the greatest risk of a poor prognosis after first-line surgery. The knockdown of sterol O-acyltransferase 1 (SOAT1)--high expression of which is a signature specific to the S-III subtype--alters the distribution of cellular cholesterol, and effectively suppresses the proliferation and migration of hepatocellular carcinoma. Finally, on the basis of a patient-derived tumour xenograft mouse model of hepatocellular carcinoma, we found that treatment with avasimibe, an inhibitor of SOAT1, markedly reduced the size of tumours that had high levels of SOAT1 expression. The proteomic stratification of early-stage hepatocellular carcinoma presented in this study provides insight into the tumour biology of this cancer, and suggests opportunities for personalized therapies that target it. Hepatocellular carcinoma is the third leading cause of deaths from cancer worldwide. Infection with the hepatitis B virus is one of the leading risk factors for developing hepatocellular carcinoma, particularly in East Asia . Although surgical treatment may be effective in the early stages, the five-year overall rate of survival after developing this cancer is only 50-70% . Here, using proteomic and phospho-proteomic profiling, we characterize 110 paired tumour and non-tumour tissues of clinical early-stage hepatocellular carcinoma related to hepatitis B virus infection. Our quantitative proteomic data highlight heterogeneity in early-stage hepatocellular carcinoma: we used this to stratify the cohort into the subtypes S-I, S-II and S-III, each of which has a different clinical outcome. S-III, which is characterized by disrupted cholesterol homeostasis, is associated with the lowest overall rate of survival and the greatest risk of a poor prognosis after first-line surgery. The knockdown of sterol O-acyltransferase 1 (SOAT1)-high expression of which is a signature specific to the S-III subtype-alters the distribution of cellular cholesterol, and effectively suppresses the proliferation and migration of hepatocellular carcinoma. Finally, on the basis of a patient-derived tumour xenograft mouse model of hepatocellular carcinoma, we found that treatment with avasimibe, an inhibitor of SOAT1, markedly reduced the size of tumours that had high levels of SOAT1 expression. The proteomic stratification of early-stage hepatocellular carcinoma presented in this study provides insight into the tumour biology of this cancer, and suggests opportunities for personalized therapies that target it. Hepatocellular carcinoma is the third leading cause of deaths from cancer worldwide. Infection with the hepatitis B virus is one of the leading risk factors for developing hepatocellular carcinoma, particularly in East Asia1. Although surgical treatment may be effective in the early stages, the five-year overall rate of survival after developing this cancer is only 50-70%2. Here, using proteomic and phospho-proteomic profiling, we characterize 110 paired tumour and non-tumour tissues of clinical early-stage hepatocellular carcinoma related to hepatitis B virus infection. Our quantitative proteomic data highlight heterogeneity in early-stage hepatocellular carcinoma: we used this to stratify the cohort into the subtypes S-I, S-II and S-III, each of which has a different clinical outcome. S-III, which is characterized by disrupted cholesterol homeostasis, is associated with the lowest overall rate of survival and the greatest risk of a poor prognosis after first-line surgery. The knockdown of sterol O-acyltransferase 1 (SOAT1)-high expression of which is a signature specific to the S-III subtype-alters the distribution of cellular cholesterol, and effectively suppresses the proliferation and migration of hepatocellular carcinoma. Finally, on the basis of a patient-derived tumour xenograft mouse model of hepatocellular carcinoma, we found that treatment with avasimibe, an inhibitor of SOAT1, markedly reduced the size of tumours that had high levels of SOAT1 expression. The proteomic stratification of early-stage hepatocellular carcinoma presented in this study provides insight into the tumour biology of this cancer, and suggests opportunities for personalized therapies that target it.Hepatocellular carcinoma is the third leading cause of deaths from cancer worldwide. Infection with the hepatitis B virus is one of the leading risk factors for developing hepatocellular carcinoma, particularly in East Asia1. Although surgical treatment may be effective in the early stages, the five-year overall rate of survival after developing this cancer is only 50-70%2. Here, using proteomic and phospho-proteomic profiling, we characterize 110 paired tumour and non-tumour tissues of clinical early-stage hepatocellular carcinoma related to hepatitis B virus infection. Our quantitative proteomic data highlight heterogeneity in early-stage hepatocellular carcinoma: we used this to stratify the cohort into the subtypes S-I, S-II and S-III, each of which has a different clinical outcome. S-III, which is characterized by disrupted cholesterol homeostasis, is associated with the lowest overall rate of survival and the greatest risk of a poor prognosis after first-line surgery. The knockdown of sterol O-acyltransferase 1 (SOAT1)-high expression of which is a signature specific to the S-III subtype-alters the distribution of cellular cholesterol, and effectively suppresses the proliferation and migration of hepatocellular carcinoma. Finally, on the basis of a patient-derived tumour xenograft mouse model of hepatocellular carcinoma, we found that treatment with avasimibe, an inhibitor of SOAT1, markedly reduced the size of tumours that had high levels of SOAT1 expression. The proteomic stratification of early-stage hepatocellular carcinoma presented in this study provides insight into the tumour biology of this cancer, and suggests opportunities for personalized therapies that target it. Hepatocellular carcinoma is the third leading cause of deaths from cancer worldwide. Infection with the hepatitis B virus is one of the leading risk factors for developing hepatocellular carcinoma, particularly in East Asia.sup.1. Although surgical treatment may be effective in the early stages, the five-year overall rate of survival after developing this cancer is only 50-70%.sup.2. Here, using proteomic and phospho-proteomic profiling, we characterize 110 paired tumour and non-tumour tissues of clinical early-stage hepatocellular carcinoma related to hepatitis B virus infection. Our quantitative proteomic data highlight heterogeneity in early-stage hepatocellular carcinoma: we used this to stratify the cohort into the subtypes S-I, S-II and S-III, each of which has a different clinical outcome. S-III, which is characterized by disrupted cholesterol homeostasis, is associated with the lowest overall rate of survival and the greatest risk of a poor prognosis after first-line surgery. The knockdown of sterol O-acyltransferase 1 (SOAT1)--high expression of which is a signature specific to the S-III subtype--alters the distribution of cellular cholesterol, and effectively suppresses the proliferation and migration of hepatocellular carcinoma. Finally, on the basis of a patient-derived tumour xenograft mouse model of hepatocellular carcinoma, we found that treatment with avasimibe, an inhibitor of SOAT1, markedly reduced the size of tumours that had high levels of SOAT1 expression. The proteomic stratification of early-stage hepatocellular carcinoma presented in this study provides insight into the tumour biology of this cancer, and suggests opportunities for personalized therapies that target it. A subtype of early-stage hepatocellular carcinoma characterized by disrupted cholesterol homeostasis and associated with a poor prognosis responds to treatment with the SOAT1 inhibitor avasimibe in a patient-derived xenograft mouse model. Hepatocellular carcinoma is the third leading cause of deaths from cancer worldwide. Infection with the hepatitis B virus is one of the leading risk factors for developing hepatocellular carcinoma, particularly in East Asia 1 . Although surgical treatment may be effective in the early stages, the five-year overall rate of survival after developing this cancer is only 50–70% 2 . Here, using proteomic and phospho-proteomic profiling, we characterize 110 paired tumour and non-tumour tissues of clinical early-stage hepatocellular carcinoma related to hepatitis B virus infection. Our quantitative proteomic data highlight heterogeneity in early-stage hepatocellular carcinoma: we used this to stratify the cohort into the subtypes S-I, S-II and S-III, each of which has a different clinical outcome. S-III, which is characterized by disrupted cholesterol homeostasis, is associated with the lowest overall rate of survival and the greatest risk of a poor prognosis after first-line surgery. The knockdown of sterol O-acyltransferase 1 (SOAT1)—high expression of which is a signature specific to the S-III subtype—alters the distribution of cellular cholesterol, and effectively suppresses the proliferation and migration of hepatocellular carcinoma. Finally, on the basis of a patient-derived tumour xenograft mouse model of hepatocellular carcinoma, we found that treatment with avasimibe, an inhibitor of SOAT1, markedly reduced the size of tumours that had high levels of SOAT1 expression. The proteomic stratification of early-stage hepatocellular carcinoma presented in this study provides insight into the tumour biology of this cancer, and suggests opportunities for personalized therapies that target it. A subtype of early-stage hepatocellular carcinoma characterized by disrupted cholesterol homeostasis and associated with a poor prognosis responds to treatment with the SOAT1 inhibitor avasimibe in a patient-derived xenograft mouse model. |
| Audience | Academic |
| Author | Zhou, Jian Xing, Baocai Li, Chaoying Sun, Aihua Huang, Cheng Zhu, Xiaodong Qian, Xiaohong Yang, Xinrong Zhao, Yang Ren, Liangliang Ying, Wantao Wang, Mingchao Sun, Huichuan Sun, Yanjun Zhang, Menghuan Fan, Jia He, Fuchu Liu, Wei Xie, Lu Shi, Tieliu Zhu, Weimin Zhang, Li Qin, Jun Tian, Fang Xu, Huali Qin, Guangrong Hu, Bo Yan, Meng Qiu, Yang Sun, Wei Huang, Yin Chen, Ning Wu, Zhenyu Liu, Mingwei Jiang, Ying Zhou, Jinan Zhao, Yan Zhang, Manli |
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Lifeomics – sequence: 5 givenname: Huichuan surname: Sun fullname: Sun, Huichuan organization: Department of Liver Surgery & Transplantation, Liver Cancer Institute and Zhongshan Hospital, Fudan University – sequence: 6 givenname: Xinrong surname: Yang fullname: Yang, Xinrong organization: Department of Liver Surgery & Transplantation, Liver Cancer Institute and Zhongshan Hospital, Fudan University – sequence: 7 givenname: Baocai surname: Xing fullname: Xing, Baocai organization: Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Peking University Cancer Hospital & Institute – sequence: 8 givenname: Wei surname: Sun fullname: Sun, Wei organization: State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics – sequence: 9 givenname: Liangliang surname: Ren fullname: Ren, Liangliang organization: State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics – sequence: 10 givenname: Bo surname: Hu fullname: Hu, Bo organization: Department of Liver Surgery & Transplantation, Liver Cancer Institute and Zhongshan Hospital, Fudan University – sequence: 11 givenname: Chaoying surname: Li fullname: Li, Chaoying organization: State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics – sequence: 12 givenname: Li surname: Zhang fullname: Zhang, Li organization: Center for Bioinformatics and Computational Biology, and the Institute of Biomedical Sciences, School of Life Sciences, East China Normal University – sequence: 13 givenname: Guangrong surname: Qin fullname: Qin, Guangrong organization: Shanghai Center for Bioinformation Technology, Shanghai Academy of Science and Technology – sequence: 14 givenname: Menghuan surname: Zhang fullname: Zhang, Menghuan organization: Shanghai Center for Bioinformation Technology, Shanghai Academy of Science and Technology – sequence: 15 givenname: Ning surname: Chen fullname: Chen, Ning organization: State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics – sequence: 16 givenname: Manli surname: Zhang fullname: Zhang, Manli organization: State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics – sequence: 17 givenname: Yin surname: Huang fullname: Huang, Yin organization: State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics – sequence: 18 givenname: Jinan surname: Zhou fullname: Zhou, Jinan organization: State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute 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of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics – sequence: 24 givenname: Cheng surname: Huang fullname: Huang, Cheng organization: Department of Liver Surgery & Transplantation, Liver Cancer Institute and Zhongshan Hospital, Fudan University – sequence: 25 givenname: Meng surname: Yan fullname: Yan, Meng organization: State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics – sequence: 26 givenname: Mingchao surname: Wang fullname: Wang, Mingchao organization: State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics – sequence: 27 givenname: Wei surname: Liu fullname: Liu, Wei organization: Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Peking University Cancer Hospital & Institute – sequence: 28 givenname: Fang surname: Tian fullname: Tian, Fang organization: State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics – sequence: 29 givenname: Huali surname: Xu fullname: Xu, Huali organization: State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics – sequence: 30 givenname: Jian surname: Zhou fullname: Zhou, Jian organization: Department of Liver Surgery & Transplantation, Liver Cancer Institute and Zhongshan Hospital, Fudan University – sequence: 31 givenname: Zhenyu surname: Wu fullname: Wu, Zhenyu organization: State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics – sequence: 32 givenname: Tieliu surname: Shi fullname: Shi, Tieliu organization: Center for Bioinformatics and Computational Biology, and the Institute of Biomedical Sciences, School of Life Sciences, East China Normal University – sequence: 33 givenname: Weimin surname: Zhu fullname: Zhu, Weimin organization: State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics – sequence: 34 givenname: Jun surname: Qin fullname: Qin, Jun organization: State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics – sequence: 35 givenname: Lu surname: Xie fullname: Xie, Lu organization: Shanghai Center for Bioinformation Technology, Shanghai Academy of Science and Technology – sequence: 36 givenname: Jia surname: Fan fullname: Fan, Jia email: fan.jia@zs-hospital.sh.cn organization: Department of Liver Surgery & Transplantation, Liver Cancer Institute and Zhongshan Hospital, Fudan University – sequence: 37 givenname: Xiaohong surname: Qian fullname: Qian, Xiaohong email: qianxh1@163.com organization: State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, College of Life Science and Bioengineering, Beijing University of Technology – sequence: 38 givenname: Fuchu surname: He fullname: He, Fuchu email: hefc@nic.bmi.ac.cn organization: State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30814741$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Contributor | Yang, Fuquan Chen, Xiangmei Sun, Yuna Wu, Zhixing Zhang, Lijuan Cai, Sanjun Chen, Zhuchu Sun, Yulin Zi, Jin Yang, Xiaoming Ying, Wantao Chen, Xiulan Liu, Siqi Zhao, Qingchuan Fan, Jia Qian, Juying Tan, Minjia Zhu, Weimin Chen, Lin Qin, Jun Shen, Huali Jiang, Bo Wang, Tong Lou, Xiaomin Liu, Qiongming Lin, Liang Wang, Quanli Jiang, Ying Xiao, Ting Dong, Jun Zeng, Rong Shen, Zhongyang Xing, Baocai Li, Zesong Cheng, Shujun Gao, Youhe Zhang, Yi Qian, Xiaohong Zhen, Bei Wang, Guangshun Wu, Yi Sun, Huichuan Hong, Tao Mao, Yousheng Zhu, Yunping Zhao, Xiaohang He, Fuchu Qin, Weisong Yang, Dong Li, Zijian Wu, Di Deng, Haiteng Shen, Lin Chen, Xinguo Sun, Wei Wang, Yi Wu, Zhenyu Chen, Anqing Cai, Jianqiang Liu, Wanlin Yang, Pengyuan |
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| Copyright | The Author(s), under exclusive licence to Springer Nature Limited 2019 COPYRIGHT 2019 Nature Publishing Group Copyright Nature Publishing Group Mar 14, 2019 |
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| PublicationDate | 2019-03-00 |
| PublicationDateYYYYMMDD | 2019-03-01 |
| PublicationDate_xml | – month: 03 year: 2019 text: 2019-03-00 |
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| PublicationSubtitle | International weekly journal of science |
| PublicationTitle | Nature (London) |
| PublicationTitleAbbrev | Nature |
| PublicationTitleAlternate | Nature |
| PublicationYear | 2019 |
| Publisher | Nature Publishing Group UK Nature Publishing Group |
| Publisher_xml | – name: Nature Publishing Group UK – name: Nature Publishing Group |
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| Snippet | Hepatocellular carcinoma is the third leading cause of deaths from cancer worldwide. Infection with the hepatitis B virus is one of the leading risk factors... |
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| Title | Proteomics identifies new therapeutic targets of early-stage hepatocellular carcinoma |
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