Dysfunction of PLA2G6 and CYP2C44-associated network signals imminent carcinogenesis from chronic inflammation to hepatocellular carcinoma
文献类型:期刊论文
作者 | Li, Meiyi1,2,3; Li, Chen1,2; Liu, Wei-Xin1,4,5; Liu, Conghui1,2,5; Cui, Jingru1,2; Li, Qingrun1,2; Ni, Hong1,2; Wu, Chaochao1,2; Chen, Chunlei1,2; Zeng, Tao1,2 |
刊名 | JOURNAL OF MOLECULAR CELL BIOLOGY |
出版日期 | 2017 |
卷号 | 9期号:6页码:489-503 |
ISSN号 | 1674-2788 |
关键词 | Cancer-related Inflammation Activated Receptor-alpha Induced Liver-injury C-myc Integrated Database Cell-proliferation Dysplastic Nodules Edge Biomarkers Trp Channels Hepatitis-b |
DOI | 10.1093/jmcb/mjx021 |
文献子类 | Article |
英文摘要 | Little is known about how chronic inflammation contributes to the progression of hepatocellular carcinoma (HCC), especially the initiation of cancer. To uncover the critical transition from chronic inflammation to HCC and the molecular mechanisms at a network level, we analyzed the time-series proteomic data of woodchuck hepatitis virus/c-myc mice and age-matched wt-C57BL/6 mice using our dynamical network biomarker (DNB) model. DNB analysis indicated that the 5th month after birth of transgenic mice was the critical period of cancer initiation, just before the critical transition, which is consistent with clinical symptoms. Meanwhile, the DNB-associated network showed a drastic inversion of protein expression and coexpression levels before and after the critical transition. Two members of DNB, PLA2G6 and CYP2C44, along with their associated differentially expressed proteins, were found to induce dysfunction of arachidonic acid metabolism, further activate inflammatory responses through inflammatory mediator regulation of transient receptor potential channels, and finally lead to impairments of liver detoxification and malignant transition to cancer. As a c-Myc target, PLA2G6 positively correlated with c-Myc in expression, showing a trend from decreasing to increasing during carcinogenesis, with the minimal point at the critical transition or tipping point. Such trend of homologous PLA2G6 and c-Myc was also observed during human hepatocarcinogenesis, with the minimal point at high-grade dysplastic nodules (a stage just before the carcinogenesis). Our study implies that PLA2G6 might function as an oncogene like famous c-Myc during hepatocarcinogenesis, while downregulation of PLA2G6 and c-Myc could be a warning signal indicating imminent carcinogenesis. |
电子版国际标准刊号 | 1759-4685 |
WOS研究方向 | Cell Biology |
语种 | 英语 |
WOS记录号 | WOS:000425284600006 |
版本 | 出版稿 |
源URL | [http://202.127.25.143/handle/331003/3395] |
专题 | 生化所2018年发文 |
通讯作者 | Wu, Jiarui; Zeng, Rong; Chen, Luonan |
作者单位 | 1.Chinese Acad Sci, Innovat Ctr Cell Signaling Network, Key Lab Syst Biol,Inst Biochem & Cell Biol, CAS Ctr Excellence Mol Cell Sci,Shanghai Inst Bio, Shanghai, Peoples R China; 2.Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell Biol, Shanghai, Peoples R China; 3.Fudan Univ, Minhang Hosp, Shanghai, Peoples R China; 4.ShanghaiTech Univ, Sch Life Sci & Technol, Shanghai, Peoples R China; 5.Univ Chinese Acad Sci, Beijing, Peoples R China; 6.Second Mil Med Univ, Eastern Hepatobiliary Surg Inst, Int Cooperat Lab Signal Transduct, Shanghai, Peoples R China; 7.Natl Ctr Liver Canc, Shanghai, Peoples R China; 8.Chinese Acad Sci, Shanghai Adv Res Inst, Shanghai, Peoples R China |
推荐引用方式 GB/T 7714 | Li, Meiyi,Li, Chen,Liu, Wei-Xin,et al. Dysfunction of PLA2G6 and CYP2C44-associated network signals imminent carcinogenesis from chronic inflammation to hepatocellular carcinoma[J]. JOURNAL OF MOLECULAR CELL BIOLOGY,2017,9(6):489-503. |
APA | Li, Meiyi.,Li, Chen.,Liu, Wei-Xin.,Liu, Conghui.,Cui, Jingru.,...&Chen, Lei.(2017).Dysfunction of PLA2G6 and CYP2C44-associated network signals imminent carcinogenesis from chronic inflammation to hepatocellular carcinoma.JOURNAL OF MOLECULAR CELL BIOLOGY,9(6),489-503. |
MLA | Li, Meiyi,et al."Dysfunction of PLA2G6 and CYP2C44-associated network signals imminent carcinogenesis from chronic inflammation to hepatocellular carcinoma".JOURNAL OF MOLECULAR CELL BIOLOGY 9.6(2017):489-503. |
入库方式: OAI收割
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