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      Lipid metabolism analysis in esophageal cancer and associated drug discovery

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          Abstract

          Esophageal cancer is an upper gastrointestinal malignancy with a bleak prognosis. It is still being explored in depth due to its complex molecular mechanisms of occurrence and development. Lipids play a crucial role in cells by participating in energy supply, biofilm formation, and signal transduction processes, and lipid metabolic reprogramming also constitutes a significant characteristic of malignant tumors. More and more studies have found esophageal cancer has obvious lipid metabolism abnormalities throughout its beginning, progress, and treatment resistance. The inhibition of tumor growth and the enhancement of antitumor therapy efficacy can be achieved through the regulation of lipid metabolism. Therefore, we reviewed and analyzed the research results and latest findings for lipid metabolism and associated analysis techniques in esophageal cancer, and comprehensively proved the value of lipid metabolic reprogramming in the evolution and treatment resistance of esophageal cancer, as well as its significance in exploring potential therapeutic targets and biomarkers.

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          Highlights

          • •

            The molecular characteristics of esophageal cancer through lipid metabolism is explored.

          • •

            Potential therapeutic targets or biomarkers related to lipid metabolism is analyzed.

          • •

            The analysis technology of lipid metabolism in esophageal cancer is summarized.

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          Global cancer statistics 2020: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries

          Hyuna Sung, Jacques Ferlay, Rebecca Siegel … (2021)
          This article provides an update on the global cancer burden using the GLOBOCAN 2020 estimates of cancer incidence and mortality produced by the International Agency for Research on Cancer. Worldwide, an estimated 19.3 million new cancer cases (18.1 million excluding nonmelanoma skin cancer) and almost 10.0 million cancer deaths (9.9 million excluding nonmelanoma skin cancer) occurred in 2020. Female breast cancer has surpassed lung cancer as the most commonly diagnosed cancer, with an estimated 2.3 million new cases (11.7%), followed by lung (11.4%), colorectal (10.0 %), prostate (7.3%), and stomach (5.6%) cancers. Lung cancer remained the leading cause of cancer death, with an estimated 1.8 million deaths (18%), followed by colorectal (9.4%), liver (8.3%), stomach (7.7%), and female breast (6.9%) cancers. Overall incidence was from 2-fold to 3-fold higher in transitioned versus transitioning countries for both sexes, whereas mortality varied <2-fold for men and little for women. Death rates for female breast and cervical cancers, however, were considerably higher in transitioning versus transitioned countries (15.0 vs 12.8 per 100,000 and 12.4 vs 5.2 per 100,000, respectively). The global cancer burden is expected to be 28.4 million cases in 2040, a 47% rise from 2020, with a larger increase in transitioning (64% to 95%) versus transitioned (32% to 56%) countries due to demographic changes, although this may be further exacerbated by increasing risk factors associated with globalization and a growing economy. Efforts to build a sustainable infrastructure for the dissemination of cancer prevention measures and provision of cancer care in transitioning countries is critical for global cancer control.
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            Ferroptosis: an iron-dependent form of nonapoptotic cell death.

            Scott J. Dixon, Kathryn Lemberg, Michael Lamprecht … (2012)
            Nonapoptotic forms of cell death may facilitate the selective elimination of some tumor cells or be activated in specific pathological states. The oncogenic RAS-selective lethal small molecule erastin triggers a unique iron-dependent form of nonapoptotic cell death that we term ferroptosis. Ferroptosis is dependent upon intracellular iron, but not other metals, and is morphologically, biochemically, and genetically distinct from apoptosis, necrosis, and autophagy. We identify the small molecule ferrostatin-1 as a potent inhibitor of ferroptosis in cancer cells and glutamate-induced cell death in organotypic rat brain slices, suggesting similarities between these two processes. Indeed, erastin, like glutamate, inhibits cystine uptake by the cystine/glutamate antiporter (system x(c)(-)), creating a void in the antioxidant defenses of the cell and ultimately leading to iron-dependent, oxidative death. Thus, activation of ferroptosis results in the nonapoptotic destruction of certain cancer cells, whereas inhibition of this process may protect organisms from neurodegeneration. Copyright © 2012 Elsevier Inc. All rights reserved.
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              A SIMPLE METHOD FOR THE ISOLATION AND PURIFICATION OF TOTAL LIPIDES FROM ANIMAL TISSUES

              Jordi Folch, M. Lees, G.H. Stanley (1957)
              Article 0 comments Cited 2084 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Luhua Wang
                Chao Zhao
                Journal
                Journal ID (nlm-ta): J Pharm Anal
                Journal ID (iso-abbrev): J Pharm Anal
                Title: Journal of Pharmaceutical Analysis
                Publisher: Xi'an Jiaotong University
                ISSN (Print): 2095-1779
                ISSN (Electronic): 2214-0883
                Publication date PMC-release: 01 September 2023
                Publication date (Print): January 2024
                Publication date (Electronic): 01 September 2023
                Volume: 14
                Issue: 1
                Pages: 1-15
                Affiliations
                [a ]Bionic Sensing and Intelligence Center, Institute of Biomedical and Health Engineering, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong, 518000, China
                [b ]Department of Radiation Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital & Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shenzhen, Guangdong, 518116, China
                [c ]School of Medicine, Southern University of Science and Technology, Shenzhen, Guangdong, 518000, China
                [d ]University of Chinese Academy of Sciences, Beijing, 100049, China
                [e ]Shenzhen Key Laboratory of Precision Diagnosis and Treatment of Depression, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong, 518000, China
                Author notes
                [∗ ]Corresponding author. Bionic Sensing and Intelligence Center, Institute of Biomedical and Health Engineering, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong, 518000, China. chao.zhao@ 123456siat.ac.cn
                [∗∗ ]Corresponding author. Department of Radiation Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital & Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shenzhen, Guangdong, 518116, China. wangluhua@ 123456csco.org.cn
                Article
                Publisher Item ID: S2095-1779(23)00211-3
                DOI: 10.1016/j.jpha.2023.08.019
                PMC ID: 10859535
                PubMed ID: 38352954
                SO-VID: 3dfd9c74-ac98-4585-a734-a36aefa59ee3
                Copyright © © 2023 The Authors
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 3 April 2023
                Date revision received : 27 July 2023
                Date accepted : 29 August 2023
                Categories
                Subject: Review Paper

                Keywords: lipid metabolism,esophageal cancer,progression,treatment resistance,new therapeutic targets
                Data availability:
                Keywords: lipid metabolism, esophageal cancer, progression, treatment resistance, new therapeutic targets

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