脂代谢重编程与原发性肝癌发生发展的关系

李飞燕; 王明刚; 毛德文; 张日云; 王娜; 罗银冰; 刘晓萍; 林玉培

doi:10.12449/JCH240829

脂代谢重编程与原发性肝癌发生发展的关系

DOI: 10.12449/JCH240829

1.
广西中医药大学研究生院，南宁 530200
2a.
广西中医药大学第一附属医院科研部，南宁 530023
2b.
广西中医药大学第一附属医院肝病科，南宁 530023

基金项目:

国家自然科学基金 (82274434);

国家自然科学基金 (81960841);

国家自然科学基金 (82060848);

广西自然科学基金 (2020GXNSFBA297115);

广西自然科学基金 (2020GXNSFAA297070);

广西中医药大学博士启动基金 (2020BS026);

广西中医药大学第一附属医院博士启动基金 (2020BS003);

广西研究生教育创新计划项目 (YCSW2023378);

广西研究生教育创新计划项目 (YCBZ2023157);

广西研究生教育创新计划项目 (YCSW2023384);

广西中医药大学研究生教育创新计划项目 (YCSY2022024);

广西高校中青年教师科研基础能力提升项目 (2022KY0284);

广西高校中青年教师科研基础能力提升项目 (2023KY0324)

利益冲突声明：本文不存在任何利益冲突。

作者贡献声明：王明刚负责研究思路的设计；罗银冰、林玉培、刘晓萍负责查阅相关文献；张日云、王娜负责资料归纳和分析；李飞燕负责撰写论文；毛德文负责指导修改论文及最后定稿。

详细信息

通信作者:
王明刚， wmgyx2012@163.com （ORCID： 0000-0002-2781-6777）

计量
- 文章访问数: 117
- HTML全文浏览量: 63
- PDF下载量: 21
- 被引次数: 0
出版历程
- 收稿日期: 2023-09-28
- 录用日期: 2023-11-08
- 出版日期: 2024-08-25

Association of lipid metabolism reprogramming with the development and progression of primary liver cancer

1.
Graduate School，Guangxi University of Chinese Medicine，Nanning 530200，China
2a.
Department of Scientific Research，The First Affiliated Hospital of Guangxi University of Chinese Medicine Nanning 530023，China
2b.
Department of Hepatology，The First Affiliated Hospital of Guangxi University of Chinese Medicine，Nanning 530023，China

Research funding:

National Natural Science Foundation of China (82274434);

National Natural Science Foundation of China (81960841);

National Natural Science Foundation of China (82060848);

Guangxi Natural Science Foundation (2020GXNSFBA297115);

Guangxi Natural Science Foundation (2020GXNSFAA297070);

Doctoral Start-up Fund of Guangxi University of Chinese Medicine (2020BS026);

The First Affiliated Hospital of Guangxi University of Chinese Medicine Doctoral Start-up Fund (2020BS003);

Innovation Project of Guangxi Graduate Education (YCSW2023378);

Innovation Project of Guangxi Graduate Education (YCBZ2023157);

Innovation Project of Guangxi Graduate Education (YCSW2023384);

Innovation Project of Guangxi Graduate Education of GXUCM (YCSY2022024);

Project on Enhancement of Basic Research Ability of Young and Middle-aged Teachers in Guangxi Universities and Colleges (2022KY0284);

Project on Enhancement of Basic Research Ability of Young and Middle-aged Teachers in Guangxi Universities and Colleges (2023KY0324)

More Information

Corresponding author: WANG Minggang， wmgyx2012@163.com （ORCID： 0000-0002-2781-6777）

摘要

摘要: 脂质代谢作为维持生命之本，是保持细胞存活的前提，脂质稳态能迅速对代谢变化做出协调反应。在癌症发生发展过程中，为了满足质膜合成和能量产生，癌细胞的脂质代谢会升高。脂质代谢异常对原发性肝癌的进展起着重要作用。本文综述二者之间的关联，以期寻找进一步防治原发性肝癌的靶点。
- 肝肿瘤 /
- 脂类代谢 /
- 代谢重编程
Abstract: Lipid metabolism， as the basis of life maintenance， is a prerequisite for cell survival， and lipid homeostasis can rapidly respond to metabolic changes in a coordinated manner. In cancers， there is an increase in lipid metabolism in cancer cells to meet the requirements for plasma membrane synthesis and energy production. Abnormal lipid metabolism plays an important role in the progression of primary liver cancer. This article reviews the association between abnormal lipid metabolism and primary liver cancer， in order to find targets for the prevention and treatment of primary liver cancer.
- Liver Neoplasms /
- Lipid Metabolism /
- Metabolic Reprogramming

HTML全文

参考文献(40)

[1]	LI X, RAMADORI P, PFISTER D, et al. The immunological and metabolic landscape in primary and metastatic liver cancer[J]. Nat Rev Cancer, 2021, 21( 9): 541- 557. DOI: 10.1038/s41568-021-00383-9.
[2]	JIANG TT, SUN FF, ZENG Z, et al. Progress on metabolic associated fatty liver disease related liver cancer[J/CD]. Chin J Liver Dis(Electronic Version), 2022, 14( 3): 14- 17. DOI: 10.3969/j.issn.1674-7380.2022.03.004. 蒋婷婷, 孙芳芳, 曾湛, 等. 代谢相关脂肪性肝病相关肝癌研究进展[J/CD]. 中国肝脏病杂志(电子版), 2022, 14( 3): 14- 17. DOI: 10.3969/j.issn.1674-7380.2022.03.004.
[3]	SIA D, VILLANUEVA A, FRIEDMAN SL, et al. Liver cancer cell of origin, molecular class, and effects on patient prognosis[J]. Gastroenterology, 2017, 152( 4): 745- 761. DOI: 10.1053/j.gastro.2016.11.048.
[4]	CHIANG CL, CHIU KWH, CHAN KSK, et al. Sequential transarterial chemoembolisation and stereotactic body radiotherapy followed by immunotherapy as conversion therapy for patients with locally advanced, unresectable hepatocellular carcinoma(START-FIT): A single-arm, phase 2 trial[J]. Lancet Gastroenterol Hepatol, 2023, 8( 2): 169- 178. DOI: 10.1016/S2468-1253(22)00339-9.
[5]	RUFF SM, SHANNON AH, PAWLIK TM. Advances in targeted immunotherapy for hepatobiliary cancers[J]. Int J Mol Sci, 2022, 23( 22): 13961. DOI: 10.3390/ijms232213961.
[6]	CHOW A, PERICA K, KLEBANOFF CA, et al. Clinical implications of T cell exhaustion for cancer immunotherapy[J]. Nat Rev Clin Oncol, 2022, 19( 12): 775- 790. DOI: 10.1038/s41571-022-00689-z.
[7]	ALANNAN M, FAYYAD-KAZAN H, TRÉZÉGUET V, et al. Targeting lipid metabolism in liver cancer[J]. Biochemistry, 2020, 59( 41): 3951- 3964. DOI: 10.1021/acs.biochem.0c00477.
[8]	SKILL NJ, SCOTT RE, WU JM, et al. Hepatocellular carcinoma associated lipid metabolism reprogramming[J]. J Surg Res, 2011, 169( 1): 51- 56. DOI: 10.1016/j.jss.2009.09.005.
[9]	HAO Y, LI DX, XU Y, et al. Investigation of lipid metabolism dysregulation and the effects on immune microenvironments in pan-cancer using multiple omics data[J]. BMC Bioinformatics, 2019, 20( Suppl 7): 195. DOI: 10.1186/s12859-019-2734-4.
[10]	YU WN, LEI QY, YANG L, et al. Contradictory roles of lipid metabolism in immune response within the tumor microenvironment[J]. J Hematol Oncol, 2021, 14( 1): 187. DOI: 10.1186/s13045-021-01200-4.
[11]	COCKCROFT S. Mammalian lipids: Structure, synthesis and function[J]. Essays Biochem, 2021, 65( 5): 813- 845. DOI: 10.1042/EBC20200067.
[12]	GUO DL, BELL EH, MISCHEL P, et al. Targeting SREBP-1-driven lipid metabolism to treat cancer[J]. Curr Pharm Des, 2014, 20( 15): 2619- 2626. DOI: 10.2174/13816128113199990486.
[13]	REPA JJ, MANGELSDORF DJ. The role of orphan nuclear receptors in the regulation of cholesterol homeostasis[J]. Annu Rev Cell Dev Biol, 2000, 16: 459- 481. DOI: 10.1146/annurev.cellbio.16.1.459.
[14]	GUO YJ, ZHAO M, BO T, et al. Blocking FSH inhibits hepatic cholesterol biosynthesis and reduces serum cholesterol[J]. Cell Res, 2019, 29( 2): 151- 166. DOI: 10.1038/s41422-018-0123-6.
[15]	SAHA P, SHUMATE JL, CALDWELL JG, et al. Inter-domain dynamics drive cholesterol transport by NPC1 and NPC1L1 proteins[J]. Elife, 2020, 9: e57089. DOI: 10.7554/eLife.57089.
[16]	van de SLUIS B, WIJERS M, HERZ J. News on the molecular regulation and function of hepatic low-density lipoprotein receptor and LDLR-related protein 1[J]. Curr Opin Lipidol, 2017, 28( 3): 241- 247. DOI: 10.1097/MOL.0000000000000411.
[17]	LI ZY, ZHANG HF. Reprogramming of glucose, fatty acid and amino acid metabolism for cancer progression[J]. Cell Mol Life Sci, 2016, 73( 2): 377- 392. DOI: 10.1007/s00018-015-2070-4.
[18]	CHENG CM, GENG F, CHENG X, et al. Lipid metabolism reprogramming and its potential targets in cancer[J]. Cancer Commun(Lond), 2018, 38( 1): 27. DOI: 10.1186/s40880-018-0301-4.
[19]	ZHANG M, WEI TJ, ZHANG XD, et al. Targeting lipid metabolism reprogramming of immunocytes in response to the tumor microenvironment stressor: A potential approach for tumor therapy[J]. Front Immunol, 2022, 13: 937406. DOI: 10.3389/fimmu.2022.937406.
[20]	BACCI M, LORITO N, SMIRIGLIA A, et al. Fat and furious: Lipid metabolism in antitumoral therapy response and resistance[J]. Trends Cancer, 2021, 7( 3): 198- 213. DOI: 10.1016/j.trecan.2020.10.004.
[21]	CHEN EB, YI J, JIANG J, et al. Identification and validation of a fatty acid metabolism-related lncRNA signature as a predictor for prognosis and immunotherapy in patients with liver cancer[J]. BMC Cancer, 2022, 22( 1): 1037. DOI: 10.1186/s12885-022-10122-4.
[22]	TIAN W, PANG WX, GE Y, et al. Hepatocyte-generated 27-hydroxycholesterol promotes the growth of melanoma by activation of estrogen receptor alpha[J]. J Cell Biochem, 2018, 119( 3): 2929- 2938. DOI: 10.1002/jcb.26498.
[23]	LI YJ, KASIM V, YAN XS, et al. Yin Yang 1 facilitates hepatocellular carcinoma cell lipid metabolism and tumor progression by inhibiting PGC-1β-induced fatty acid oxidation[J]. Theranostics, 2019, 9( 25): 7599- 7615. DOI: 10.7150/thno.34931.
[24]	XIA LZ, OYANG L, LIN JG, et al. The cancer metabolic reprogramming and immune response[J]. Mol Cancer, 2021, 20( 1): 28. DOI: 10.1186/s12943-021-01316-8.
[25]	PAN MX, QIN C, HAN XL. Lipid metabolism and lipidomics applications in cancer research[J]. Adv Exp Med Biol, 2021, 1316: 1- 24. DOI: 10.1007/978-981-33-6785-2_1.
[26]	BROADFIELD LA, PANE AA, TALEBI A, et al. Lipid metabolism in cancer: New perspectives and emerging mechanisms[J]. Dev Cell, 2021, 56( 10): 1363- 1393. DOI: 10.1016/j.devcel.2021.04.013.
[27]	WANG MD, HAN J, XING H, et al. Dysregulated fatty acid metabolism in hepatocellular carcinoma[J]. Hepat Oncol, 2016, 3( 4): 241- 251. DOI: 10.2217/hep-2016-0012.
[28]	WANG B, ZHANG H, CHEN YF, et al. Acyl-CoA thioesterase 9 promotes tumour growth and metastasis through reprogramming of fatty acid metabolism in hepatocellular carcinoma[J]. Liver Int, 2022, 42( 11): 2548- 2561. DOI: 10.1111/liv.15409.
[29]	TOMACHA J, DOKDUANG H, PADTHAISONG S, et al. Targeting fatty acid synthase modulates metabolic pathways and inhibits cholangiocarcinoma cell progression[J]. Front Pharmacol, 2021, 12: 696961. DOI: 10.3389/fphar.2021.696961.
[30]	NATH A, LI I, ROBERTS LR, et al. Elevated free fatty acid uptake via CD36 promotes epithelial-mesenchymal transition in hepatocellular carcinoma[J]. Sci Rep, 2015, 5: 14752. DOI: 10.1038/srep14752.
[31]	XU HJ, ZHOU S, TANG QL, et al. Cholesterol metabolism: New functions and therapeutic approaches in cancer[J]. Biochim Biophys Acta Rev Cancer, 2020, 1874( 1): 188394. DOI: 10.1016/j.bbcan.2020.188394.
[32]	WANG HL, SHANG XY, WAN X, et al. Increased hepatocellular carcinoma risk in chronic hepatitis B patients with persistently elevated serum total bile acid: A retrospective cohort study[J]. Sci Rep, 2016, 6: 38180. DOI: 10.1038/srep38180.
[33]	THOMAS CE, LUU HN, WANG RW, et al. Association between pre-diagnostic serum bile acids and hepatocellular carcinoma: The Singapore Chinese health study[J]. Cancers(Basel), 2021, 13( 11): 2648. DOI: 10.3390/cancers13112648.
[34]	WANG CZ, YANG MY, ZHAO JF, et al. Bile salt(glycochenodeoxycholate acid) induces cell survival and chemoresistance in hepatocellular carcinoma[J]. J Cell Physiol, 2019, 234( 7): 10899- 10906. DOI: 10.1002/jcp.27905.
[35]	XIE GX, WANG XN, HUANG FJ, et al. Dysregulated hepatic bile acids collaboratively promote liver carcinogenesis[J]. Int J Cancer, 2016, 139( 8): 1764- 1775. DOI: 10.1002/ijc.30219.
[36]	RESSOM HW, XIAO JF, TULI L, et al. Utilization of metabolomics to identify serum biomarkers for hepatocellular carcinoma in patients with liver cirrhosis[J]. Anal Chim Acta, 2012, 743: 90- 100. DOI: 10.1016/j.aca.2012.07.013.
[37]	GAO CQ, CHU ZZ, ZHANG D, et al. Serine/threonine kinase TBK1 promotes cholangiocarcinoma progression via direct regulation of β-catenin[J]. Oncogene, 2023, 42( 18): 1492- 1507. DOI: 10.1038/s41388-023-02651-4.
[38]	PAUL B, LEWINSKA M, ANDERSEN JB. Lipid alterations in chronic liver disease and liver cancer[J]. JHEP Rep, 2022, 4( 6): 100479. DOI: 10.1016/j.jhepr.2022.100479.
[39]	SZLASA W, ZENDRAN I, ZALESIŃSKA A, et al. Lipid composition of the cancer cell membrane[J]. J Bioenerg Biomembr, 2020, 52( 5): 321- 342. DOI: 10.1007/s10863-020-09846-4.
[40]	POMYEN Y, CHAISAINGMONGKOL J, RABIBHADANA S, et al. Gut dysbiosis in Thai intrahepatic cholangiocarcinoma and hepatocellular carcinoma[J]. Sci Rep, 2023, 13( 1): 11406. DOI: 10.1038/s41598-023-38307-2.