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| 1 | Glucose metabolism in gastric cancer:The cutting-edge显示文摘Glucose metabolism in gastric cancer cells differs from that of normal epithelial cells. Upregulated aerobic glycolysis(Warburg effect) in gastric cancer meeting the demands of cell proliferation is associated with genetic mutations, epigenetic modification and proteomic alteration. Understanding the mechanisms of aerobic glycolysis may contribute to our knowledge of gastric carcinogenesis. Metabolomic studies offer novel, convenient and practical tools in the search for new biomarkers for early detection, diagnosis, prognosis, and chemosensitivity prediction of gastric cancer. Interfering with the process of glycolysis in cancer cells may provide a new and promising therapeutic strategy for gastric cancer. In this article, we present a brief review of recent studies of glucose metabolism in gastric cancer, with primary focus on the clinical applications of new biomarkers and their potential therapeutic role in gastric cancer. | Lian-Wen Yuan Hiroharu Yamashita Yasuyuki Seto | 2016 | World Journal of Gastroenterology2016，22，6： | 18 |
| 2 | Role of abnormal lipid metabolism in development,progression,diagnosis and therapy of pancreatic cancer显示文摘There is growing evidence that metabolic alterations play an important role in cancer development and progression.The metabolism of cancer cells is reprogrammed in order to support their rapid proliferation.Elevated fatty acid synthesis is one of the most important aberrations of cancer cell metabolism.An enhancement of fatty acids synthesis is required both for carcinogenesis and cancer cell survival,as inhibition of key lipogenic enzymes slows down the growth of tumor cells and impairs their survival.Based on the data that serum fatty acid synthase(FASN),also known as oncoantigen 519,is elevated in patients with certain types of cancer,its serum level was proposed as a marker of neoplasia.This review aims to demonstrate the changes in lipid metabolism and other metabolic processes associated with lipid metabolism in pancreatic ductal adenocarcinoma(PDAC),the most common pancreatic neoplasm,characterized by high mortality.We also addressed the influence of some oncogenic factors and tumor suppressors on pancreatic cancer cell metabolism.Additionally the review discusses the potential role of elevated lipid synthesis in diagnosis and treatment of pancreatic cancer.In particular,FASN is a viable candidate for indicator of pathologic state,marker of neoplasia,as well as,pharmacological treatment target in pancreatic cancer.Recent research showed that,in addition to lipogenesis,certain cancer cells can use fatty acids from circulation,derived from diet(chylomicrons),synthesized in liver,or released from adipose tissue for their growth.Thus,the interactions between de novo lipogenesis and uptake of fatty acids from circulation by PDAC cells require further investigation. | Julian Swierczynski Areta Hebanowska Tomasz Sledzinski | 2014 | World Journal of Gastroenterology2014，20，9： | 16 |
| 3 | 5-氟尿嘧啶为基础的联合化疗对结直肠癌患者血糖代谢的影响显示文摘目的:观察结直肠癌患者接受以5-氟尿嘧啶(5-fluorouracil, 5-FU)为基础的联合化疗前和化疗期间血糖水平的变化,探讨5-FU与患者发生糖尿病(diabetes mellitus, DM)之间的关系.方法:采用回顾性方法分析97例接受含5-FU方案化疗的结直肠癌患者在化疗前和化疗期间空腹血糖的变化.结果: 剔除化疗前罹患DM的3例患者、空腹血糖受损的3例患者以及糖耐量异常的1例患者,对剩余的化疗前空腹血糖正常的90例患者进行分析.其中,化疗期间继发DM者5例(5/90,5.56%),继发空腹血糖损伤者16例(16/90,17.78%),继发糖耐量损伤者1例(1/90,1.11%).5例继发DM的患者在化疗前以及化疗期间出现继发DM时的平均空腹血糖分别为(4.95±0.31)和(12.20±6.23) mmol/L,化疗后空腹血糖水平明显高于化疗前空腹血糖水平(P<0.01);继发DM时的中位5-FU累积剂量为7 500 mg/m2,至DM时的中位化疗周期数为2个;其中4例患者有糖皮质激素注射史,继发DM时的中位地塞米松累积剂量为25 mg;继发DM患者中有1例死于DM酮症酸中毒.16例继发空腹血糖损伤的患者中,12例患者在化疗结束2~7个月后空腹血糖恢复至正常,其余4例仍维持空腹血糖损伤状态,短期随访无一例演变为DM.结论:以5-FU为基础的化疗可诱使结直肠癌患者继发DM,甚至可引起DM酮症酸中毒.部分患者出现一过性空腹血糖受损. | 冯觉平 方静 袁响林 李敏 王亚萍 骆曼 | 2010 | 肿瘤2010，30，10： | 15 |
| 4 | Dysregulated lipid metabolism in cancer显示文摘Alteration of lipid metabolism has been increasingly recognized as a hallmark of cancer cells. The changes of expression and activity of lipid metabolizing enzymes are directly regulated by the activity of oncogenic signals. The dependence of tumor cells on the dysregulated lipid metabolism suggests that proteins involved in this process are excellent chemotherapeutic targets for cancer treatment. There are currently several drugs under development or in clinical trials that are based on specifically targeting the altered lipid metabolic pathways in cancer cells. Further understanding of dysregulated lipid metabolism and its associated signaling pathways will help us to better design efficient cancer therapeutic strategy. | Feng Zhang Guang-Wei Du | 2012 | World Journal of Biological Chemistry2012，3，8： | 12 |
| 5 | Glycolysis reprogramming in cancer-associated fibroblasts promotes the growth of oral cancer through the lncRNA H19/miR-675-5p/PFKFB3 signaling pathway显示文摘As an important component of the tumor microenvironment,cancer-associated fibroblasts(CAFs)secrete energy metabolites to supply energy for tumor progression.Abnormal regulation of long noncoding RNAs(lncRNAs)is thought to contribute to glucose metabolism,but the role of lncRNAs in glycolysis in oral CAFs has not been systematically examined.In the present study,by using RNA sequencing and bioinformatics analysis,we analyzed the lncRNA/mRNA profiles of normal fibroblasts(NFs)derived from normal tissues and CAFs derived from patients with oral squamous cell carcinoma(OSCC).LncRNA H19 was identified as a key lncRNA in oral CAFs and was synchronously upregulated in both oral cancer cell lines and CAFs.Using small interfering RNA(siRNA)strategies,we determined that lncRNA H19 knockdown affected proliferation,migration,and glycolysis in oral CAFs.We found that knockdown of lncRNA H19 by siRNA suppressed the MAPK signaling pathway,6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3(PFKFB3)and miR-675-5p.Furthermore,the lncRNA H19/miR-675-5p/PFKFB3 axis was involved in promoting the glycolysis pathway in oral CAFs,as demonstrated by a luciferase reporter system assay and treatment with a miRNA-specific inhibitor.Our study presents a new way to understand glucose metabolism in oral CAFs,theoretically providing a novel biomarker for OSCC molecular diagnosis and a new target for antitumor therapy. | Jin Yang Xueke Shi Miao Yang Jingjing Luo Qinghong Gao Xiangjian Wang Yang Wu Yuan Tian Fanglong Wu Hongmei Zhou | 2021 | International Journal of Oral Science2021，13，1： | 8 |
| 6 | Oxidative stress: the lowest common denominator of multiple diseases显示文摘Oxygen is essential to the human life and life of all aerobic organisms. The complete oxidation of nutrients for the biological energy supply is one of the most important prerequisites for the formation of higher life forms. However, cells that benefit from oxidative respiration also suffer from reactive oxygen species because they adapted to oxygen as an energy source. Healthy cells balance the formation and elimination of reactive oxygen species thereby creating and keeping reactive oxygen species-homeostasis. When the concentration of free radicals exceeds a critical level and homeostasis is disturbed, oxidative stress occurs leading to damage of multiple cellular molecules and compartments. Therefore, oxidative stress plays an important role in the physiology and pathology of various diseases. Often, the antioxidant protection system becomes pathologically unbalanced in the genesis of several diseases, leading to functional losses of the organism, as in the case of amyotrophic lateral sclerosis, or cells develop metabolic mechanisms to use this system as protection against external influences, such as in the case of glioblastoma cells. Either way, understanding the underlying deregulated mechanisms of the oxidative protection system would allow the development of novel treatment strategies for various diseases. Thus, regardless of the direction in which the reactive oxygen species-homeostasis disequilibrate, the focus should be on the oxidative protection system. | Veronika Matschke Carsten Theiss Johann Matschke | 2019 | Neural Regeneration Research2019，14，2： | 7 |
| 7 | Metabolism and disposition of pyrotinib in healthy male volunteers: covalent binding with human plasma protein显示文摘Pyrotinib is a novel irreversible EGFR/HER2 dual tyrosine kinase inhibitor that is used to treat HER2-positive breast cancer. In this study we investigated the metabolism and disposition of pyrotinib in six healthy Chinese men after a single oral dose of 402?mg of [14C]pyrotinib. At 240?h postdose, the mean cumulative excretion of the dose radioactivity was 92.6%, including 1.7% in urine and 90.9% in feces. In feces, oxidative metabolites were detected as major drug-related materials and the primary metabolic pathways were O-depicoline (M1), oxidation of pyrrolidine (M5), and oxidation of pyridine (M6-1, M6-2, M6-3, and M6-4). In plasma, the major circulating entities identified were pyrotinib, SHR150980 (M1), SHR151468 (M2), and SHR151136 (M5), accounting for 10.9%, 1.9%, 1.0%, and 3.0%, respectively, of the total plasma radioactivity based on the AUC0–∞ ratios. Approximately 58.3% of the total plasma radioactivity AUC0–∞ was attributed to covalently bound materials. After incubation of human plasma with [14C]pyrotinib at 37?°C for 2, 5, 8, and 24?h, the recovery of radioactivity by extraction was 97.4%, 91.8%, 69.6%, and 46.7%, respectively, revealing covalent binding occurred independently of enzymes. A group of pyrotinib adducts, including pyrotinib-lysine and pyrotinib adducts of the peptides Gly-Lys, Lys-Ala, Gly-Lys-Ala, and Lys-Ala-Ser, was identified after HCl hydrolysis of the incubated plasma. Therefore, the amino acid residue Lys190 of human serum albumin was proposed to covalently bind to pyrotinib via Michael addition. Finally, the covalently bound pyrotinib could dissociate from the human plasma protein and be metabolized by oxidation and excreted via feces. | Jian Meng Xiao-yun Liu Sheng Ma Hua Zhang Song-da Yu Yi-fan Zhang Mei-xia Chen Xiao-yu Zhu Yi Liu Ling Yi Xiao-liang Ding Xiao-yan Chen Li-yan Miao Da-fang Zhong | 2019 | Acta Pharmacologica Sinica2019，40，7： | 7 |
| 8 | Mitochondria as therapeutic targets for cancer stem cells显示文摘Cancer stem cells(CSCs) are maintained by theirsomatic stem cells and are responsible for tumor initiation, chemoresistance, and metastasis. Evidence for the CSCs existence has been reported for a number of human cancers. The CSC mitochondria have been shown recently to be an important target for cancer treatment, but clinical significance of CSCs and their mitochondria properties remain unclear. Mitochondriatargeted agents are considerably more effective compared to other agents in triggering apoptosis of CSCs, as well as general cancer cells, via mitochondrial dysfunction. Mitochondrial metabolism is altered in cancer cells because of their reliance on glycolytic intermediates, which are normally destined for oxidative phosphorylation. Therefore, inhibiting cancer-specific modifications in mitochondrial metabolism, increasing reactive oxygen species production, or stimulating mitochondrial permeabilization transition could be promising new therapeutic strategies to activate cell death in CSCs as well, as in general cancer cells. This review analyzed mitochondrial function and its potential as a therapeutic target to induce cell death in CSCs. Furthermore, combined treatment with mitochondriatargeted drugs will be a promising strategy for the treatment of relapsed and refractory cancer. | In Sung Song Jeong Yu Jeong Seung Hun Jeong Hyoung Kyu Kim Kyung Soo Ko Byoung Doo Rhee Nari Kim Jin Han | 2015 | World Journal of Stem Cells2015，7，2： | 4 |
| 9 | Significance of long non-coding RNA AGPG for the metabolism of esophageal cancer显示文摘Over the years,thousands of long non-coding RNAs(lncRNAs)have been identified to be exclusively expressed in specific cancer types and for their unique functions in tumorigenesis.This has led to an increasing interest in elucidating the vital roles[1]and underlying mechanism[2,3]of such non-coding genome in driving cancerous phenotypes.A number of studies have pinpointed the key functions of lncRNAs in diverse biological events including chromatin interactions,transcriptional regulation,RNA processing,mRNA stabilization,signal transduction,and metabolic regulation;highlighting their essential roles in both physiology and diseases such as cancer[4]. | Rebecca Elizabeth Vargas Wenqi Wang | 2020 | Cancer Communications2020，40，7： | 4 |
| 10 | AMPK promotes the survival of colorectal cancer stem cells显示文摘Background: Colorectal cancer(CRC) is the third most commonly diagnosed cancer in males and the second in females worldwide in 2012. In the past 20 years, strong evidence suggests that cancer stem cells are the main culprit of cancer metastasis,chemotherapy resistance, and relapse.Methods: To further understand the unique biological properties of cancer stem cells and uncover novel molecular targets to eradicate them, we first established a panel of patient-derived xenograft(PDX) tumor models using tumors surgically removed from human colorectal cancer patients. We then isolated CRC cancer stem cells based on their ALDH activity using fluorescent-activated cell sorting(FACS)and characterized their metabolic properties.Results: Interestingly, we found that the CRC cancer stem cells(ie, CRC cells with higher ALDH activity, or ALDH+) express higher level of antioxidant genes and have lower level of reactive oxygen species(ROS) than non-CRC cancer stem cells(ie, CRC cells with lower ALDH activity, or ALDHà). The CRC cancer stem cells also possess more mitochondria mass and show higher mitochondrial activity. More intriguingly,we observed higher AMP-activated protein kinase(AMPK) activities in these CRC cancer stem cells. Inhibition of the AMPK activity using 2 AMPK inhibitors, Compound C and Iodotubercidin, preferentially induces cell death in CRC cancer stem cells.Conclusion: We propose that AMPK inhibitors may help to eradicate the CRC cancer stem cells and prevent the relapse of CRCs. | Bing Guo Xin Han Diane Tkach Shu-Guang Huang Dong Zhang | 2018 | Animal Models and Experimental Medicine2018，1，2： | 3 |
| 11 | Alcohol consumption on pancreatic diseases显示文摘Although the association between alcohol and pancreatic diseases has been recognized for a long time,the impact of alcohol consumption on pancreatitis and pancreatic cancer(PC)remains poorly defined.Nowadays there is not consensus about the epidemiology and the beverage type,dose and duration of alcohol consumption causing these diseases.The objective of this study was to review the epidemiology described in the literature for pancreatic diseases as a consequence of alcoholic behavior trying to understand the association between dose,type and frequency of alcohol consumption and risk of pancreatitis and PC.The majority of the studies conclude that high alcohol intake was associated with a higher risk of pancreatitis(around 2.5%-3% between heavy drinkers and 1.3%between non drinkers).About 70%of pancreatitis are due to chronic heavy alcohol consumption.Although this incidence rate differs between countries,it is clear that the risk of developing pancreatitis increases with increasing doses of alcohol and the average of alcohol consumption vary since 80 to 150 g/d for 10-15 years.With regard to PC, the role of alcohol consumption remains less clear,and low to moderate alcohol consumption do not appear to be associated with PC risk,and only chronic heavy drinking increase the risk compared with lightly drinkers.In a population of 10%-15%of heavy drinkers, 2%-5%of all PC cases could be attributed to alcohol consumption.However,as only a minority(less than 10%for pancreatitis and 5%for PC)of heavily drinkers develops these pancreatic diseases,there are other predisposing factors besides alcohol involved.Genetic variability and environmental exposures such as smoking and diet modify the risk and should be considered for further investigations. | Marta Herreros-Villanueva Elizabeth Hijona Jesus Maria Baales Angel Cosme Luis Bujanda | 2013 | World Journal of Gastroenterology2013，19，5： | 3 |
| 12 | THZ1 suppresses human non-small-cell lung cancer cells in vitro through interference with cancer metabolism显示文摘Cancer cells always require more nutrients, energy, and biosynthetic activity to sustain their rapid proliferation than normal cells. Previous studies have shown the impact of THZ1, a covalerrt inhibitor of ryHirwjependent kinase 7 (CDK7), on transcription regulation and cell-cycle arrest in numerous (nncers, but its effects on cellular metabolism in cancer colls remain unknown. In this btudy we elucidated the anticancer mechanism of THZ1 in human non-small-cell lung cancer (NSCLC) cells. We showed that treatment with THZ1 (10 1000 nM) dose-dependently suppressed the proliferation of human NSCLC cell lines H1299, A549, H292, and H23, and markedly inhibited the migration of these NSCLC cells. Furthermore treatment with THZ1 (50 nM) arrested cell cycle at G2/M phase and induced apoptosis in these NSCLC cell lines. More importantly, we revealed that treatment with THZ1 (50 nM) blocked the glycolysis pathway but had no effect on glutamine metabolism. Wc further demonstrated that THZ1 treatment altered thp expression pattern of gluwminasc 1 (GLS1) Isoforms through promoting the ubiquitination and degradation of NUDT21. Combined treatment of THZ1 with a glutaminase inhibitor CB-839 (500 nM) exerted a more potent anti-proliferative effect in these NSCLC cell lines than treatment with TH21 or CB-83Q alone. Our results demonstrate that the inhibitory effect of THZ1 on the growth of humnn NSCLC cells is partially attributed to interfering with cancer metabolism. Thus, we provide a new potential therapeutic strategy for NSCLC treatment by combining THZ1 with the inhibitors of glutamine metabolism. | Zhu-Jun Cheng Du-Ling Miao Qiu-Yun Su Xiao-Li Tang Xiao-Lei Wang Li Bin Deng Hui Donq Shi Hong-Bo Xin | 2019 | Acta Pharmacologica Sinica2019，40，6： | 3 |
| 13 | MiR-22 as a metabolic silencer and liver tumor suppressor显示文摘With obesity rate consistently increasing,a strong relationship between obesity and fatty liver disease has been discovered.More than 90%of bariatric surgery patients also have non-alcoholic fatty liver diseases(NAFLDs).NAFLD and non-alcoholic steatohepatitis(NASH),which are the hepatic manifesta-tions of metabolic syndrome,can lead to liver carcinogenesis.Unfortunately,there is no effective medicine that can be used to treat NASH or liver cancer.Thus,it is critically important to understand the mechanism underlying the development of these diseases.Extensive evidence suggests that microRNA 22(miR-22)can be a diagnostic marker for liver diseases as well as a treatment target.This review paper focuses on the roles of miR-22 in metabolism,steatosis,and liver carcinogenesis.Literature search is limited based on the publications included in the PubMed database in the recent 10 years. | Lijun Wang Yu-Shiuan Wang Eko Mugiyanto Wei-Chiao Chang Yu-Jui Yvonne Wan | 2020 | Liver Research2020，4，2： | 3 |
| 14 | Molecular predictors of gemcitabine response in pancreatic cancer显示文摘Gemcitabine is one of the most used anti-neoplastic drugs with documented activity in almost all major localizations of cancer.In pancreatic cancer treatment,gemcitabine occupies a prominent place as a first line chemotherapy,partly because of the paucity of other efficacious chemotherapy options.In fact,only a minority of pancreatic cancer patients display a response or even stability of disease with the drug.There are currently no clinically applicable means of predicting which patient will derive a clinical benefit from gemcitabine although several proposed markers have been studied. These markers are proteins involved in drug up-take,activation and catabolism or proteins that define the ability of the cell to undergo apoptosis in response to the drug.Several of these markers are reviewed in this paper.We also briefly discuss the possible role of stem cells in drug resistance to gemcitabine. | Ioannis A Voutsadakis | 2011 | World Journal of Gastrointestinal Oncology2011，3，11： | 3 |
| 15 | The therapeutic implications of immunosuppressive tumor aerobic glycolysis显示文摘In 2011,Hanahan and Weinberg added“Deregulating Cellular Energetics”and“Avoiding Immune Destruction”to the six previous hallmarks of cancer.Since this seminal paper,there has been a growing consensus that these new hallmarks are not mutually exclusive but rather interdependent.The following review summarizes how founding genetic events for tumorigenesis ultimately increase tumor cell glycolysis,which not only supports the metabolic demands of malignancy but also provides an immunoprotective niche,promoting malignant cell proliferation,maintenance and progression.The mechanisms by which altered metabolism contributes to immune impairment are multifactorial:(1)the metabolic demands of proliferating tumor cells and activated immune cells are similar,thus creating a situation where immune cells may be in competition for key nutrients;(2)the metabolic byproducts of aerobic glycolysis directly inhibit antitumor immunity while promoting a regulatory immune phenotype;and(3)the gene programs associated with the upregulation of glycolysis also result in the generation of immunosuppressive cytokines and metabolites.From this perspective,we shed light on important considerations for the development of new classes of agents targeting cancer metabolism.These types of therapies can impair tumor growth but also pose a significant risk of stifling antitumor immunity. | Bradley I.Reinfeld WKimryn Rathmell Tae Kon Kim Jeffrey C.Rathmell | 2022 | Cellular & Molecular Immunology2022，19，1： | 3 |
| 16 | Targeting metabolism in breast cancer: How far we can go?显示文摘Adjuvant therapies for breast cancer have achieved great success in recent years and early breast cancer is now a curable or chronic disease. Targeted therapies, including endocrine therapy and human epidermal growth factor receptor-2 targeted therapy, marked a new era of breast cancer treatment. However, except for chemotherapy, an efficient drug treatment to improve the overall survival of breast cancer patients is still lacking for triple negative breast cancer. Furthermore, a certain proportion of breast cancer patients present with resistance to drug therapy, making it much more difficult to control the deterioration of the disease. Recently, altered energy metabolism has become one of the hallmarks of cancer, including breast cancer, and it may be linked to drug resistance. Targeting cellular metabolism is becoming a promising strategy to overcome drug resistance in cancer therapy. This review discusses metabolic reprogramming in breast cancer and the possible complex mechanism of modulation. We also summarize the recent advances in metabolic therapy targeted glycolysis, glutaminolysis and fatty acids synthesis in breast cancer. | Jing-Pei Long Xiao-Na Li Feng Zhang | 2016 | World Journal of Clinical Oncology2016，7，1： | 2 |
| 17 | Metabolic regulation of immune responses to cancer显示文摘The tumor microenvironment is an ecosystem composed of multiple types of cells, such as tumor cells, immune cells, and cancerassociated fibroblasts. Cancer cells grow faster than non-cancerous cells and consume larger amounts of nutrients. The rapid growth characteristic of cancer cells fundamentally alters nutrient availability in the tumor microenvironment and results in reprogramming of immune cell metabolic pathways. Accumulating evidence suggests that cellular metabolism of nutrients, such as lipids and amino acids, beyond being essential to meet the bioenergetic and biosynthetic demands of immune cells, also regulates a broad spectrum of cellular signal transduction, and influences immune cell survival, differentiation, and anti-tumor effector function. The cancer immunometabolism research field is rapidly evolving, and exciting new discoveries are reported in high-profile journals nearly weekly. Therefore, all new findings in this field cannot be summarized within this short review. Instead, this review is intended to provide a brief introduction to this rapidly developing research field, with a focus on the metabolism of two classes of important nutrients-lipids and amino acids-in immune cells. We highlight recent research on the roles of lipids and amino acids in regulating the metabolic fitness and immunological functions of T cells, macrophages, and natural killer cells in the tumor microenvironment. Furthermore, we discuss the possibility of “editing” metabolic pathways in immune cells to act synergistically with currently available immunotherapies in enhancing anti-tumor immune responses. | Jannis WiBfeld Anke Werner Xin Yan Nora ten Bosch Guoliang Cui | 2022 | Cancer Biology & Medicine2022，19，11： | 2 |
| 18 | Regulation of cancer cell metabolism:oncogenic MYC in the driver’s seat显示文摘Cancer cells must rewire cellular metabolism to satisfy the demands of unbridled growth and proliferation.As such,most human cancers differ from normal counterpart tissues by a plethora of energetic and metabolic reprogramming.Transcription factors of the MYC family are deregulated in up to 70%of all human cancers through a variety of mechanisms.Oncogenic levels of MYC regulates almost every aspect of cellular metabolism,a recently revisited hallmark of cancer development.Meanwhile,unrestrained growth in response to oncogenic MYC expression creates dependency on MYC-driven metabolic pathways,which in principle provides novel targets for development of effective cancer therapeutics.In the current review,we summarize the significant progress made toward understanding how MYC deregulation fuels metabolic rewiring in malignant transformation. | Yang Dong Rongfu Tu Hudan Liu Guoliang Qing | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 2 |
| 19 | Nanosecond pulsed electric feld interrupts the glycogen metabolism in hepatocellular carcinoma by modifying the osteopontin pathway显示文摘To the Editor:Hepatocellular carcinoma (HCC) is one of the most common lethal cancers and is the leading cause of cancer mortality worldwide [1].In recent years,developments in locoregional therapies have provided new options for the treatment of HCC,which are recommended by the international guidelines including the Barcelona Clinic Liver Cancer (BCLC) and the American Joint Committee on Cancer (AJCC)[2]. | Shen Hu Yan Zhu Yu Chen Pu Cheng Gui-Rong Wang Li-Quan Wang Xin-Mei Chen | 2022 | Hepatobiliary & Pancreatic Diseases International2022，21，2： | 2 |
| 20 | Dysregulated ceramides metabolism by fatty acid 2-hydroxylase exposes a metabolic vulnerability to target cancer metastasis显示文摘Whereas it is appreciated that cancer cells rewire lipid metabolism to survive and propagate,the roles of lipid metabolism in metastasis remain largely unknown.In this study,using esophageal squamous cell carcinoma(ESCC)as a pulmonary metastasis model,we find that the enzyme fatty acid 2-hydroxylase(FA2H),which catalyzes the hydroxylation of free fatty acids(FAs),is enriched in a subpopulation of ESCC cells with high metastatic potential,and that FA2H knockdown markedly mitigates metastatic lesions.Moreover,increased FA2H expression is positively associated with poor survival in patients with ESCC.Lipidomics analysis identifies that two dihydroceramides—Cer(d18:0/24:0)and Cer(d18:0/24:1)—are increased in FA2H-depleted metastasizing ESCC cells.Upon administration,Cer(d18:0/24:0)and Cer(d18:0/24:1)impair the formation of overt metastases in a mouse experimental metastasis model.Then,forkhead box protein C2(FOXC2)and FA2H are found to be co-upregulated in metastatic ESCC cell populations and ESCC specimens,and FA2H expression is further experimentally verified to be transcriptionally induced by FOXC2,which is boosted per se by tumour necrosis factorα(TNFα),a critical pro-metastasis cytokine in the tumour microenvironment,in metastasizing cells.Together,these results demonstrate that TNFα-FOXC2-FA2H is a novel signaling axis to promote metastasis,and its downstream dihydroceramide products could be promising drugs to intervene in metastasis. | Xuantong Zhou Furong Huang Gang Ma Wenqing Wei Nan Wu Zhihua Liu | 2022 | Signal Transduction and Targeted Therapy2022，7，11： | 2 |
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