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Low expression of fatty acid oxidation related gene ACADM indicates poor prognosis of renal clear cell carcinoma and is related to tumor immune infltration

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Oncology Research 2024年第3期32卷 545-561页

作者： JIECHUAN QIU TIANMIN YANG YANNING SUN KAI SUN YINGKUN XU QINGHUA XIA Department of Urology Shandong Provincial Hospital A fliated to Shandong First Medical UniversityJinan250021China Depatment of Urology Shandong Provincial HospitalCheeloo College of MedicineShandong UniversityJinan250021China Depatment of Breast and Thyroid Surgery The First Afiliated Hospital of Chongqing Medical UniversityChongqing400042China

This research aims to identify the key fatty acid beta-oxidation(FAO)genes that are altered in kidney renal clear cell carcinoma(KIRC)and to analyze the role of these genes in KIRC The Gene Expression Omnibus(GEO)and FAO datasets were used to identify these key *** rank sum test was used to assess the levels of acyl-CoA dehydrogenase medium chain(ACADM)between KIRC and non cancer *** logistic regression and Wilcoxon rank sum test were used to explore the association between ACADM and clinical *** diagnostic performance of ACADM for KIRC was asessed using a diagnostic receiver operating ch aracteristic(ROC)*** co-expressed genes of ACADM were identifed in LinkedOmics database,and their function and pathway enrichment were *** correlation between ACADM expression level and immune infitration was analyzed by Gene Set Variation Analysis(GSVA)method Additionally,the proliferation,migration,and invasion abilities of KIRC cells were assessed after overexpressing *** differential analysis and intersection,we identifed six hub genes,induding *** found that the expression level of ACADM was decreased in KIRC tissues and had a better diagnostic efect(AUC=0.916).Survival analysis suggested that patients with decreased ACADM expression had a worse *** to correlation analysis,a variety of dinical features were associated with the expression level of ACADML By analyzing the infiltration level of immune cells,we found that ACADM may be related to the enrichment of immune ***,ACADM overexpression inhibited proliferation,migration,and invasion of KIRC *** conclusion,our findings suggest that reduced ACADM expression in KIRC patients is indicative of poor *** results imply that ACADM may be a diagnostic and prognostic marker for individuals with KIRC,offering a reference for dinicians in diagnosis and treatment.

关键词： Kidney renal clear cell carcinoma Acyl CoA dehydrogenase medium chain Immune infiltration fatty acid oxidation Prognosis

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fatty acid oxidation and autophagy promote endoxifen resistance and counter the effect of AKT inhibition in ER-positive breast cancer cells

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Journal of Molecular Cell Biology 2021年第6期13卷 433-444页

作者： Lei Duan Sarah Calhoun Daeun Shim Ricardo E.Perez Lothar A.Blatter Carl G.Maki Department of Cell and Molecular Medicine Rush University Medical CenterChicagoIL 60612USA Department of Molecular Biophysics and Physiology Rush University Medical CenterChicagoIL 60612USA

Tamoxifen(TAM)is the first-line endocrine therapy for estrogen receptor-positive(ER+)breast cancer(BC).However,acquired resistance occurs in∼50%***,although the PI3K/AKT/mTOR pathway is a viable target for treatment of endocrine therapy-refractory patients,complex signaling feedback loops exist,which can counter the effectiveness of inhibitors of this ***,we analyzed signaling pathways and metabolism in ER+MCF7 BC cell line and their TAM-resistant derivatives that are co-resistant to endoxifen using immunoblotting,quantitative polymerase chain reaction,and the Agilent Seahorse XF *** found that activation of AKT and the energy-sensing kinase AMPK was increased in TAM and endoxifen-resistant ***,ERRα/PGC-1βand their target genes MCAD and CPT-1 were increased and regulated by AMPK,which coincided with increased fatty acid oxidation(FAO)and autophagy in TAM-resistant *** of AKT feedback-activates AMPK and ERRα/PGC-1β-MCAD/CPT-1 with a consequent increase in FAO and autophagy that counters the therapeutic effect of endoxifen and AKT ***,our results indicate increased activation of AKT and AMPK with metabolic reprogramming and increased autophagy in TAM-resistant *** inhibition of AKT and FAO/autophagy is necessary to fully sensitize resistant cells to endoxifen.

关键词： endoxifen fatty acid oxidation autophagy AMPK AKT

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Rhodiola crenulata extract decreases fatty acid oxidation and autophagy to ameliorate pulmonary arterial hypertension by targeting inhibiton of acylcarnitine in rats

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Chinese Journal of Natural Medicines 2021年第2期19卷 120-133页

作者： REN Huan-Huan NIU Zheng GUO Rui FU Min LI Hai-Ru ZHANG Xuan-Yu YAO Li Department of Medicinal Chemistry and Natural Medicine Chemistry Department of PharmacognosyCollege of PharmacyHarbin Medical UniversityHarbin 150081China State-Province Key Laboratory of Biomedicine-Pharmaceutics of China Harbin Medical UniversityHarbin 150081China Key Laboratory of Systems Biomedicine(Ministry of Education) Shanghai Center for Systems BiomedicineShanghai Jiao Tong UniversityShanghai 200240China Department of Ultrasound The Second Affiliated Hospital of Harbin Medical UniversityHarbin 150081China

Pulmonary arterial hypertension(PAH)is a devastating pulmonary circulation disease lacking high-efficiency *** present study aims to decipher the therapeutic mechanism of Rhodiola crenulata,a well-known traditional chinese medicine with cardiopulmonary protection capacity,on PAH by exploiting functional *** rat model with PAH was successfully established for first,following Rhodiola crenulata water extract(RCE)treatment,then analysis of chemical constituents of RCE was performed,additional morphologic,hemodynamic,echocardiographic measurements were examined,further targeted lipidomics assay was performed to identify differential lipidomes,at last accordingly mechanism assay was done by combining qRT-PCR,Western blot and *** lipidomes were identified and characterized to differentiate the rats with PAH from healthy controls,mostly assigned to acylcarnitines,phosphatidylcholines,sphingomyelin associated with the PAH ***,RCE administration reversed high level of decadienyl-L-carnitine by the modulation of metabolic enzyme CPT1A in mRNA and protein level in serum and lung in the rats with ***,RCE was observed to reduce autophagy,confirmed by significantly inhibited PPARγ,LC3B,ATG7 and upregulated p62,and inactivated LKB1-AMPK signal ***,we accurately identified the constituents in RCE,and delineated the therapeutic mechansim that RCE ameliorated PAH through inhibition of fatty acid oxidation and ***,RCE might be a potential therapeutic medicine with multi-targets characteristics to prevent the progression of *** novel findings pave a critical foundation for the use of RCE in the treatment of PAH.

关键词： Pulmonary arterial hypertension Rhodiola crenulata Target lipidomics fatty acid oxidation Autophagy

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Glycolytic and fatty acid oxidation genes affect the treatment and prognosis of liver cancer

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World Journal of Clinical Cases 2022年第15期10卷 4737-4760页

作者： Jia-Yue Zou Yu-Jie Huang Jun He Zu-Xiong Tang Lei Qin Department of General Surgery The First Affiliated Hospital of Soochow UniversitySuzhou 215006Jiangsu ProvinceChina

BACKGROUND Metabolic reprogramming is a feature of tumour cells and is essential to support their rapid *** glycolytic activity of liver cancer cells is significantly higher than that of normal liver cells,and the rapidly proliferating tumour cells are powered by aerobic *** metabolism reprogramming enables tumour cells to meet their needs for highly proliferative growth and is an important driving force for the development of hepatocellular carcinoma(HCC).AIM To explore the influence of different metabolic subtypes of HCC and analyse their significance in guiding prognosis and treatment based on the molecular mechanism of glycolysis and fatty acid oxidation(FAO).METHODS By downloading related data from public databases including the Cancer Genome Atlas(TCGA),the Molecular Signatures Database,and International Cancer Genome Consortium,we utilised unsupervised consensus clustering to divide TCGA Liver Hepatocellular Carcinoma samples into four metabolic subgroups and compared single nucleotide polymorphism,copy number variation,tumour microenvironment,and Genomics of Drug Sensitivity in Cancer and Tumour Immune Dysfunction and Exclusion between different *** differences and causes of survival and the clinical characteristics between them were analysed,and a prognostic model was established based on glycolysis and FAO *** with the clinical features,a Norman diagram was created to compare the pros and cons of each *** In the four metabolic subgroups,with the increase in glycolytic expression,the median survival of patients showed the worst results,while FAO showed the *** comparing the follow-up analysis of each group,we considered that the differences between them might be related to reactive oxygen species,somatic copy number variation of key genes,and immune *** was also found that the FAO group and the low-risk group had better efficacy and response to immune checkpoint blockade treat

关键词： Metabolic reprogramming fatty acid oxidation Tumour immune dysfunction and exclusion Hepatocellular carcinoma Nomogram

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Inhibition of nitric oxide synthase lowers fatty acid oxidation in ~reeclampsia-like mice at early gestational stage

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Chinese Medical Journal 2011年第19期 3141-3147页

作者： MA Rui-qiong SUN Min-na YANG Zi Department of Obstetrics and Gynecology Peking University Third Hospital Beijing 100191 China

Background Preeclampsia is one of hypertensive disorders in pregnancy. It is associated with abnormal lipid metabolism, including fatty acid oxidation metabolism. Long chain 3-hydroxyacyI-CoA dehydrogenase （LCHAD） plays an indispensable role in the oxidation of fatty acids. It has been reported that nitric oxide （NO） is one of the regulatory factors of the fatty acid oxidation pathway. The aim of this research was to investigate whether the nitric oxide synthase （NOS）inhibitor L-NAME may cause down-regulation of LCHAD in the pathogenesis of *** Pregnant wild-type （WT） mice were treated with L-NAME or normal saline （NS） during gestation days 7-18 （early group）, days 11-18 （mid group） and days 16-18 （late group）, and apoE-/- mice served as a control. Systolic blood pressure （SBP）, urine protein, feto-placental outcome, plasma lipid levels and NO concentrations were measured, and the expression of mRNA and protein for LCHAD in placental tissue were determined by real-time polymerase chain reaction （RT-PCR） and Western blotting, *** In WT and apoE-/- mice, SBP and urinary protein increased following L-NAME injection. Fetal and placental weights and NO concentrations were reduced and total cholesterol, triglycerides and free fatty acid levels were increased in early and mid L-NAME groups in WT and apoE-/- mice, compared with the NS group. There was no significant difference between the late L-NAME group and NS group. RT-PCR and Western blotting analysis showed that the mRNA and protein levels of LCHAD expression were significantly down-regulated in the early and mid L-NAME groups but not in the late L-NAME group in the WT and apoE-/- mice compared with the corresponding NS *** Inhibition of NO in early and mid gestation in mice may cause hyperlipidemia and suppression of fatty acid oxidation, whereas preeclampsia-like conditions in late gestation may be a maternal vascular response to inhibition of NO.

关键词： nitric oxide synthase preeclampsia fatty acid oxidation

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Nutritional stress promotes the induction of dormant colorectal cancer cells via regulating fatty acid oxidation

Nutritional stress promotes the induction of dormant colorec...

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第十四届全国免疫学学术大会

作者： Jing Liu Meng Zhang Ruyi Peng Haizhou Wang Zhongnan hospital of Wuhan university

Dormant cancer cells drive immune escape and recurrence, which lead to poor prognosis. Recent studies indicated that the adaptive faculty of cancer cells to nutrient limitation is one of the major factors to sustain survival during tumor progression. However, the correlation between dormant state and nutrient stress in colorectal cancer(CRC) remains unclear. Here, we showed that CRC cells can suffer from nutrient stress by entering dormant state. We further identified that nutrient stress upregulated the expression of Nanog to induce dormancy in CRC cells. Mechanistically, Nanog was regulated through a fatty acid oxidation(FAO)/ATP citrate lyase(ACLY)-dependent pathway. Enhanced FAO increased ACLY expression to promote the synthesis of acetyl-CoA, which was transferred by P300 to accelerate H3K27 acetylation of Nanog promoter. Then, Nanog upregulation increased the transcription of P21 and P27, which promoting the dormancy of CRC cells. Our findings corroborated that dormancy-enabled CRC cells survival through metabolic challenge and unlocked a specific mechanism to govern the process.

关键词： Nutrient stress dormancy Nanog fatty acid oxidation citrate lyase

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Betaine affects muscle lipid metabolism via regulating the fatty acid uptake and oxidation in finishing pig

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Journal of Animal Science and Biotechnology 2018年第1期9卷 187-195页

作者： Sisi Li Haichao Wang Xinxia Wang Yizhen Wang Jie Feng Key Laboratory of Animal Nutrition & Feed Zhejiang Province College of Animal Science Zhejiang University

Background： Betaine affects fat metabolism in animals, but the specific mechanism is still not clear. The purpose of this study was to investigate possible mechanisms of betaine in altering lipid metabolism in muscle tissue in finishing ***： A total of 120 crossbred gilts（Landrace × Yorkshire × Duroc） with an average initial body weight of 70.1 kg were randomly allotted to three dietary treatments. The treatments included a corn–soybean meal basal diet supplemented with 0, 1250 or 2500 mg/kg betaine. The feeding experiment lasted 42 ***： Betaine addition to the diet significantly increased the concentration of free fatty acids（FFA） in muscle（P 〈 0.05）. Furthermore, the levels of serum cholesterol and high-density lipoprotein cholesterol were decreased（P 〈 0.05） and total cholesterol content was increased in muscle（P 〈 0.05） of betaine fed pigs. Experiments on genes involved in fatty acid transport showed that betaine increased expression of lipoprotein lipase（LPL）, fatty acid translocase/cluster of differentiation（FAT/CD36）, fatty acid binding protein（FABP3） and fatty acid transport protein（FATP1）（P 〈 0.05）. The abundance of fatty acid transport protein and fatty acid binding protein were also increased by betaine（P 〈 0.05）. As for the key factors involved in fatty acid oxidation, although betaine supplementation didn＇t affect the level of carnitine and malonyl-CoA, betaine increased mR NA and protein abundance of carnitine palmitransferase-1（CPT1）and phosphorylated-AMPK（P 〈 0.05）.Conclusions： The results suggested that betaine may promoted muscle fatty acid uptake via up-regulating the genes related to fatty acid transporter including FAT/CD36, FATP1 and FABP3. On the other hand, betaine activated AMPK and up-regulated genes related to fatty acid oxidation including PPARα and CPT1. The underlying mechanism regulating fatty acid metabolism in pigs supplemented with betaine is associated with the up-regulation of genes involved in fatty acid transport

关键词： Betaine fatty acid intake fatty acid oxidation Muscle Pig

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Metabolic reprogramming of the inflammatory response in the nervous system:the crossover between inflammation and metabolism

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Neural Regeneration Research 2024年第10期19卷 2189-2201页

作者： Jesus Amo-Aparicio Charles A.Dinarello Ruben Lopez-Vales Department of Medicine University of ColoradoAuroraCOUSA Institute of Neurosciences and Department Cell BiologyPhysiology and ImmunologyUniversitat Autònoma de BarcelonaBellaterraSpain Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas(CIBERNED) Instituto de Salud Carlos ⅢSpain

Metabolism is a fundamental process by which biochemicals are broken down to produce energy(catabolism) or used to build macromolecules(anabolism). Metabolism has received renewed attention as a mechanism that generates molecules that modulate multiple cellular responses. This was first identified in cancer cells as the Warburg effect, but it is also present in immunocompetent cells. Studies have revealed a bidirectional influence of cellular metabolism and immune cell function, highlighting the significance of metabolic reprogramming in immune cell activation and effector functions. Metabolic processes such as glycolysis, oxidative phosphorylation, and fatty acid oxidation have been shown to undergo dynamic changes during immune cell response, facilitating the energetic and biosynthetic demands. This review aims to provide a better understanding of the metabolic reprogramming that occurs in different immune cells upon activation, with a special focus on central nervous system disorders. Understanding the metabolic changes of the immune response not only provides insights into the fundamental mechanisms that regulate immune cell function but also opens new approaches for therapeutic strategies aimed at manipulating the immune system.

关键词： central nervous system fatty acid oxidation glycolysis inflammation macrophage metabolism microglia neurodegeneration oxidative phosphorylation

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Adverse effects of triclosan on kidney in mice: Implication of lipid metabolism disorders

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Journal of Environmental Sciences 2023年第2期124卷 481-490页

作者： Wei Huang Guodong Cao Chengliang Deng Yanyan Chen Tao Wang Da Chen Zongwei Cai State Key Laboratory of Environmental and Biological Analysis Hong Kong Baptist UniversityHong Kong 999077China School of Environment Guangdong Key Laboratory of Environmental Pollution and HealthJinan UniversityGuangzhou 510632China Analysis Center School of PharmacyGuangdong Medical UniversityDongguan 523808China

Triclosan(TCS)is a ubiquitous antimicrobial used in daily consumer *** reports have shown that TCS could induce hepatotoxicity,endocrine disruption,disturbance on immune function and impaired thyroid *** is critical in the elimination of toxins,while the effects of TCS on kidney have not yet been *** aim of the present study was to investigate the effects of TCS exposure on kidney function and the possible underlying mechanisms in *** C57BL/6 mice were orally exposed to TCS with the doses of 10 and 100 mg/(kg•day)for 13 *** was dissolved in dimethyl sulfoxide(DMSO)and diluted by corn oil for *** oil containing DMSO was used as vehicle *** and kidney tissues were collected for *** associated with kidney function,oxidative stress,inflammation and fibrosis were *** results showed that TCS could cause renal injury as was revealed by increased levels of renal function markers including serum creatinine,urea nitrogen and uric acid,as well as increased oxidative stress,pro-inflammatory cytokines and fibroticmarkers in a dose dependent manner,whichweremore significantly in 100 mg/(kg•day)*** spectrometry-based analysis of metabolites relatedwith lipid metabolism demonstrated the occurrence of lipid accumulation and defective fatty acid oxidation in 100 mg/(kg•day)TCS-exposed mouse *** processes might lead to lipotoxicity and energy depletion,thus resulting in kidney fibrosis and functional *** together,the present study demonstrated that TCS could induce lipid accumulation and fatty acid metabolism disturbance in mouse kidney,whichmight contribute to renal function *** present study further widens our insights into the adverse effects of TCS.

关键词： Triclosan Renal injury Lipid accumulation fatty acid oxidation

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Nonalcoholic fatty liver disease and mitochondrial dysfunction

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World Journal of Gastroenterology 2008年第2期14卷 193-199页

作者： Yongzhong Wei R Scott Rector John P Thyfault Jamal A Ibdah Division of Gastroenterology and Hepatology Harry S. Truman VA MedicalCenter Columbia MO 65212 United States Division of Gastroenterology and Hepatology Department of Nutritional Sciences University of Missouri-Columbia Harry S. Truman VA Medical Center Columbia MO65212 United States

Nonalcoholic fatty liver disease (NAFLD) includes hepatic steatosis, nonalcoholic steatohepatitis (NASH), fibrosis, and cirrhosis. NAFLD is the most common liver disorder in the United States and worldwide. Due to the rapid rise of the metabolic syndrome, the prevalence of NAFLD has recently dramatically increased and will continue to increase. NAFLD has also the potential to progress to hepatocellular carcinoma (HCC) or liver failure. NAFLD is strongly linked to caloric overconsumption, physical inactivity, insulin resistance and genetic factors. Although significant progress in understanding the pathogenesis of NAFLD has been achieved in years, the primary metabolic abnormalities leading to lipid accumulation within hepatocytes has remained poorly understood. Mitochondria are critical metabolic organelles serving as "cellular power plants". Accumulating evidence indicate that hepatic mitochondrial dysfunction is crucial to the pathogenesis of NAFLD. This review is focused on the significant role of mitochondria in the development of NAFLD.

关键词： Nonalcoholic fatty liver disease Mitochondria fatty acid oxidation Liver

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