Glycerophospholipid-driven lipid metabolic reprogramming as a common key mechanism in the progression of human primary hepatocellular carcinoma and cholangiocarcinoma.
Humans
Cholangiocarcinoma
/ metabolism
Carcinoma, Hepatocellular
/ metabolism
Liver Neoplasms
/ metabolism
Glycerophospholipids
/ metabolism
Lipid Metabolism
Male
Middle Aged
Female
Bile Duct Neoplasms
/ metabolism
Metabolomics
/ methods
Disease Progression
Phosphatidylcholines
/ metabolism
Lysophosphatidylcholines
/ metabolism
Aged
Phospholipases A2
/ metabolism
Metabolic Reprogramming
CCA
Glycerophospholipid metabolism
HCC
Metabolic reprogramming
Phospholipase A2
Journal
Lipids in health and disease
ISSN: 1476-511X
Titre abrégé: Lipids Health Dis
Pays: England
ID NLM: 101147696
Informations de publication
Date de publication:
01 Oct 2024
01 Oct 2024
Historique:
received:
18
07
2024
accepted:
13
09
2024
medline:
2
10
2024
pubmed:
2
10
2024
entrez:
1
10
2024
Statut:
epublish
Résumé
Metabolic reprogramming, a key mechanism regulating the growth and recurrence of hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA), still lacks effective clinical strategies for its integration into the precise screening of primary liver cancer. This study utilized ultra-high-performance liquid chromatography with quadrupole time-of-flight mass spectrometry to conduct a comprehensive, non-targeted metabolomics analysis, revealing significant upregulation of lipid metabolites such as phosphatidylcholine and lysophosphatidylcholine in patients with HCC and CCA, particularly within the glycerophospholipid metabolic pathway. Hematoxylin and eosin and immunohistochemical staining demonstrated marked upregulation of phospholipase A
Identifiants
pubmed: 39354487
doi: 10.1186/s12944-024-02298-4
pii: 10.1186/s12944-024-02298-4
doi:
Substances chimiques
Glycerophospholipids
0
Phosphatidylcholines
0
Lysophosphatidylcholines
0
Phospholipases A2
EC 3.1.1.4
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
326Informations de copyright
© 2024. The Author(s).
Références
Desjonqueres E, et al. Preneoplastic lesions in the liver: molecular insights and relevance for clinical practice. Liver Int. 2022;42(3):492–506.
doi: 10.1111/liv.15152
pubmed: 34982503
Calderaro J, et al. Deep learning-based phenotyping reclassifies combined hepatocellular-cholangiocarcinoma. Nat Commun. 2023;14(1):8290.
doi: 10.1038/s41467-023-43749-3
pubmed: 38092727
pmcid: 10719304
Yang F, et al. Metabolic reprogramming and its clinical implication for liver cancer. Hepatology. 2023;78(5):1602–24.
doi: 10.1097/HEP.0000000000000005
pubmed: 36626639
Raggi C, et al. Metabolic reprogramming in cholangiocarcinoma. J Hepatol. 2022;77(3):849–64.
doi: 10.1016/j.jhep.2022.04.038
pubmed: 35594992
Faubert B, Solmonson A, DeBerardinis RJ. Metabolic reprogramming and cancer progression. Science. 2020;368(6487):eaaw5473.
doi: 10.1126/science.aaw5473
pubmed: 32273439
pmcid: 7227780
Hu B, Lin JZ, Yang XB, Sang XT. Aberrant lipid metabolism in hepatocellular carcinoma cells as well as immune microenvironment: a review. Cell Prolif. 2020;53(3):e12772.
doi: 10.1111/cpr.12772
pubmed: 32003505
pmcid: 7106960
Yang K, et al. The role of lipid metabolic reprogramming in tumor microenvironment. Theranostics. 2023;13(6):1774–808.
doi: 10.7150/thno.82920
pubmed: 37064872
pmcid: 10091885
Lin J, Rao D, Zhang M, Gao Q. Metabolic reprogramming in the tumor microenvironment of liver cancer. J Hematol Oncol. 2024;17(1):6.
doi: 10.1186/s13045-024-01527-8
pubmed: 38297372
pmcid: 10832230
Anwanwan D, et al. Challenges in liver cancer and possible treatment approaches. Biochim Biophys Acta Rev Cancer. 2020;1873(1):188314.
doi: 10.1016/j.bbcan.2019.188314
pubmed: 31682895
Huang X, et al. The HGF-MET axis coordinates liver cancer metabolism and autophagy for chemotherapeutic resistance. Autophagy. 2019;15(7):1258–79.
doi: 10.1080/15548627.2019.1580105
pubmed: 30786811
pmcid: 6613896
Zhao L, et al. Impacts and mechanisms of metabolic reprogramming of tumor microenvironment for immunotherapy in gastric cancer. Cell Death Dis. 2022;13(4):378.
doi: 10.1038/s41419-022-04821-w
pubmed: 35444235
pmcid: 9021207
Dang NH, et al. Targeted cancer therapeutics: biosynthetic and energetic pathways characterized by metabolomics and the interplay with key cancer regulatory factors. Curr Pharm Des. 2014;20(15):2637–47.
doi: 10.2174/13816128113199990489
pubmed: 23859615
Han J, Li Q, Chen Y, Yang Y. Recent Metabolomics Analysis in Tumor Metabolism Reprogramming. Front Mol Biosci. 2021;8:763902.
doi: 10.3389/fmolb.2021.763902
pubmed: 34901157
pmcid: 8660977
Hall Z, et al. Lipid remodeling in hepatocyte proliferation and hepatocellular carcinoma. Hepatology. 2021;73(3):1028–44.
doi: 10.1002/hep.31391
pubmed: 32460431
de Gauna Ruiz M, et al. Cholangiocarcinoma progression depends on the uptake and metabolization of extracellular lipids. Hepatology. 2022;76(6):1617–33.
doi: 10.1002/hep.32344
Satriano L, et al. Metabolic rearrangements in primary liver cancers: cause and consequences. Nat Rev Gastroenterol Hepatol. 2019;16(12):748–66.
doi: 10.1038/s41575-019-0217-8
pubmed: 31666728
Luo Z, Eichinger KM, Zhang A, Li S. Targeting cancer metabolic pathways for improving chemotherapy and immunotherapy. Cancer Lett. 2023;575:216396.
doi: 10.1016/j.canlet.2023.216396
pubmed: 37739209
Chen S, Duan H, Sun G. Reshaping immunometabolism in the tumour microenvironment to improve cancer immunotherapy. Biomed Pharmacother. 2023;164:114963.
doi: 10.1016/j.biopha.2023.114963
pubmed: 37269814
Li H, et al. MiR-4310 regulates hepatocellular carcinoma growth and metastasis through lipid synthesis. Cancer Lett. 2021;519:161–71.
doi: 10.1016/j.canlet.2021.07.029
pubmed: 34303763
Zhang H, et al. Oleic acid-PPARγ-FABP4 loop fuels cholangiocarcinoma colonization in lymph node metastases microenvironment. Hepatology. 2024;80(1):69–86.
pubmed: 38377465
Tan SLW, et al. The altered lipidome of hepatocellular carcinoma. Semin Cancer Biol. 2022;86(Pt 3):445–56.
doi: 10.1016/j.semcancer.2022.02.004
pubmed: 35131480
Shalapour S, Karin M. Fatty acid-induced T cell loss greases liver carcinogenesis. Cell Metab. 2016;23(5):759–61.
doi: 10.1016/j.cmet.2016.04.018
pubmed: 27166937
Sonkar K, et al. Focus on the glycerophosphocholine pathway in choline phospholipid metabolism of cancer. NMR Biomed. 2019;32(10):e4112.
doi: 10.1002/nbm.4112
pubmed: 31184789
pmcid: 6803034
Law SH, et al. An updated review of lysophosphatidylcholine metabolism in human diseases. Int J Mol Sci. 2019;20(5):1149.
doi: 10.3390/ijms20051149
pubmed: 30845751
pmcid: 6429061
Vinciguerra M, et al. Unsaturated fatty acids promote hepatoma proliferation and progression through downregulation of the tumor suppressor PTEN. J Hepatol. 2009;50(6):1132–41.
doi: 10.1016/j.jhep.2009.01.027
pubmed: 19398230
Lin CR, et al. Omega-3 polyunsaturated fatty acids suppress metastatic features of human cholangiocarcinoma cells by suppressing twist. J Nutr Biochem. 2019;74:108245.
doi: 10.1016/j.jnutbio.2019.108245
pubmed: 31678746
Yun BK, et al. Potential nutritional and metabolomic advantages of high fat oral supplementation in pancreatectomized pancreaticobiliary cancer patients. Nutrients. 2019;11(4):893.
doi: 10.3390/nu11040893
pubmed: 31010058
pmcid: 6521063
Lagal DJ, et al. Loss of PRDX6 aborts proliferative and migratory signaling in hepatocarcinoma cell lines. Antioxidants (Basel). 2023;12(6):1153.
doi: 10.3390/antiox12061153
pubmed: 37371884
Ashkar F, Wu J. E-Cadherin and its signaling pathways: a novel target of dietary components in modulating cell migration and proliferation. Trends Food Sci Technol. 2024;146:104398.
doi: 10.1016/j.tifs.2024.104398
Ambesi A, McKeown-Longo PJ. Anastellin, the angiostatic fibronectin peptide, is a selective inhibitor of lysophospholipid signaling. Mol Cancer Res. 2009;7(2):255–65.
doi: 10.1158/1541-7786.MCR-08-0195
pubmed: 19208746
pmcid: 2658630
Hou R, et al. Targeting EP2 receptor with multifaceted mechanisms for high-risk neuroblastoma. Cell Rep. 2022;39(12):111000.
doi: 10.1016/j.celrep.2022.111000
pubmed: 35732130
pmcid: 9282716
Ferreira MT, et al. Cyclooxygenase inhibition alters proliferative, migratory, and invasive properties of human glioblastoma cells in vitro. Int J Mol Sci. 2021;22(9):4297.
doi: 10.3390/ijms22094297
pubmed: 33919029
pmcid: 8122446