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Aberrant LETM1 elevation dysregulates mitochondrial functions and energy metabolism and promotes lung metastasis in osteosarcoma

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Genes & Diseases 2024年第3期11卷 368-384页

作者： Yulu Shi Quan Kang Hong Zhou Xiaohan Yue Yang Bi Qing Luo stem cell Biology and therapy Laboratory The Children's Hospital of Chongqing Medical UniversityNational Clinical Research Center for Child Health and DisordersMinistry of Education Key Laboratory of Child Development and DisordersChongqing Key Laboratory of PediatricsChongqing 400014China Department of Pediatric Surgery The Children's Hospital of Chongqing Medical UniversityChongqing 400014China

Osteosarcoma is a differentiation-deficient disease,and despite the unique advan-tages and great potential of differentiation therapy,there are only a few known differentia-tion inducers,and little research has been done on their targets.cell differentiation is associated with an increase in mitochondrial content and activity.The metabolism of some tu-mor cells is characterized by impaired oxidative phosphorylation,as well as up-regulation of aerobic glycolysis and pentose phosphate pathways.Leucine-containing zipper and EF-hand transmembrane protein 1(LETM1)is involved in the maintenance of mitochondrial morphology and is closely associated with tumorigenesis and progression,as well as cancer cell stemness.We found that MG63 and 143B osteosarcoma cells overexpress LETM1 and exhibit abnormalities in mitochondrial structure and function.Knockdown of LETM1 partially restored the mitochon-drial structure and function,inhibited the pentose phosphate pathway,promoted oxidative phosphorylation,and led to osteogenic differentiation.It also inhibited spheroid cell forma-tion,proliferation,migration,and invasion in an in vitro model.When LETM1 was knocked down in vivo,there was reduced tumor formation and lung metastasis.These data suggest that mitochondria are aberrant in LETM1-overexpressing osteosarcoma cells,and knockdown of LETM1 partially restores the mitochondrial structure and function,inhibits the pentose phosphate pathway,promotes oxidative phosphorylation,and increases osteogenic differentiation,thereby reducing malignant biological behavior of the cells.

关键词： Cancer metabolism Differentiation LETM1 Osteosarcoma stemness

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Lactate regulates major zygotic genome activation by H3K18 lactylation in mammals

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National Science Review 2024年第2期11卷 124-134页

作者： Jingyu Li Weibo Hou Qi Zhao Wei Han Hongdi Cui Songling Xiao Ling Zhu Jiadan Qu Xiaoyu Liu Weitao Cong Jingling Shen Yuzheng Zhao Shaorong Gao Guoning Huang Qingran Kong chongqing Key Laboratory of Human Embryo engineering Center for Reproductive Medicine Chongqing Health Center for Women and ChildrenWomen and Children's Hospital of Chongqing Medical University Oujiang Laboratory Zhejiang Provincial Key Laboratory of Medical Genetics Key Laboratory of Laboratory MedicineMinistry of EducationSchool of Laboratory Medicine and Life Sciences Wenzhou Medical University Frontier Science center for stem cell research School of Life Sciences and Technology Tongji University School of Pharmaceutical Science Wenzhou Medical University Institute of Life Sciences College of Life and Environmental Sciences Wenzhou University Optogenetics&Synthetic Biology Interdisciplinary research center State Key Laboratory of Bioreactor Engineering Shanghai Frontiers Science Center of Optogenetic Techniques for Cell Metabolism School of Pharmacy East China University of Science and Technology

Lactate is present at a high level in the microenvironment of mammalian preimplantation embryos in vivo and in vitro. However, its role in preimplantation development is unclear. Here, we report that lactate is highly enriched in the nuclei of early embryos when major zygotic genome activation(ZGA) occurs in humans and mice. The inhibition of its production and uptake results in developmental arrest at the 2-cell stage, major ZGA failure, and loss of lactate-derived H3K18lac, which could be rescued by the addition of Lac-Co A and recapitulated by overexpression of H3K18R mutation. By profiling the landscape of H3K18lac during mouse preimplantation development, we show that H3K18lac is enriched on the promoter regions of most major ZGA genes and correlates with their expressions. In humans, H3K18lac is also enriched in ZGA markers and temporally concomitant with their expressions. Taken together, we profile the landscapes of H3K18lac in mouse and human preimplantation embryos, and demonstrate the important role for H3K18lac in major ZGA, showing that a conserved metabolic mechanism underlies preimplantation development of mammalian embryos.

关键词： mammalian preimplantation development lactate epigenetic remodeling histone lactylation zygotic genome activation

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Dual-Defect engineering Strategy Enables High-Durability Rechargeable Magnesium-Metal Batteries

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Nano-Micro Letters 2024年第9期16卷 449-461页

作者： Fuyu Chen Bai‑Qing Zhao Kaifeng Huang Xiu‑Fen Ma Hong‑Yi Li Xie Zhang Jiang Diao Jili Yue Guangsheng Huang Jingfeng Wang Fusheng Pan National Innovation center for Lndustry‑Education Integration of Energy Storage technology School of Materials Science and EngineeringChongqing UniversityChongqing 400044People’s Republic of China National Magnesium Alloy Material engineering technology research center Chongqing UniversityChongqing 400044People’s Republic of China Materials and Energy Division Beijing Computational Science Research CenterBeijing 100193People’s Republic of China School of Materials Science and engineering Northwestern Polytechnical UniversityXi’an 710072People’s Republic of China National Key Laboratory of Advanced Casting Technologies Chongqing UniversityChongqing 400044People’s Republic of China

Rechargeable magnesium-metal batteries(RMMBs)are promising next-generation secondary batteries;however,their development is inhibited by the low capacity and short cycle lifespan of cathodes.Although various strategies have been devised to enhance the Mg^(2+)migration kinetics and structural stability of cathodes,they fail to improve electronic conductivity,rendering the cathodes incompatible with magnesium-metal anodes.Herein,we propose a dual-defect engineering strategy,namely,the incorporation of Mg^(2+)pre-intercalation defect(P-Mgd)and oxygen defect(Od),to simultaneously improve the Mg^(2+)migration kinetics,structural stability,and electronic conductivity of the cathodes of RMMBs.Using lamellar V_(2)O_(5)·nH_(2)O as a demo cathode material,we prepare a cathode comprising Mg0.07V_(2)O_(5)·1.4H_(2)O nanobelts composited with reduced graphene oxide(MVOH/rGO)with P-Mgd and Od.The Od enlarges interlayer spacing,accelerates Mg^(2+)migration kinetics,and prevents structural collapse,while the P-Mgd stabilizes the lamellar structure and increases electronic conductivity.Consequently,the MVOH/rGO cathode exhibits a high capacity of 197 mAh g^(−1),and the developed Mg foil//MVOH/rGO full cell demonstrates an incredible lifespan of 850 cycles at 0.1 A g^(−1),capable of powering a light-emitting diode.The proposed dual-defect engineering strategy provides new insights into developing high-durability,high-capacity cathodes,advancing the practical application of RMMBs,and other new secondary batteries.

关键词： Rechargeable magnesium-metal batteries Dual-defect engineering Vanadium-based cathode High durability Lamellar structure

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CRISPR,CAR-T,and NK:Current applications and future perspectives

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Genes & Diseases 2024年第4期11卷 246-257页

作者： Mohadeseh Khoshandam Hossein Soltaninejad Amir Ali Hamidieh Saman Hosseinkhani Department of Reproductive Biology Academic Center for EducationCultureand Research(ACECR)Qom branch***Iran National Institute of Genetic engineering and Biotechnology(NIGEB) Tehran 14965/161Iran Department of stem cells technology and Tissue Regeneration Faculty of Interdisciplinary Science and TechnologiesTarbiat Modares UniversityTehran 15614Iran Pediatric cell therapy and Gene therapy research center GeneCell&Tissue Research InstituteTehran University of Medical SciencesTehran ***Iran Department of Biochemistry Faculty of Biological SciencesTarbiat Modares UniversityTehran 15614Iran

Chimeric antigen receptor T(CAR-T)cell therapy represents a breakthrough in personalized cancer treatments.In this regard,synthetic receptors comprised of antigen recognition domains,signaling,and stimulatory domains are used to reprogram T-cells to target tum or cells and destroy them.Despite the success of this approach in refractory B-cell malignancies,the optimal potency of CAR T-cell therapy for many other cancers,particularly solid tumors,has not been validated.Natural killer cells are powerful cytotoxic lymphocytes specialized in recognizing and dispensing the tumor cells in coordination with other anti-tumor immunity cells.Based on these studies,many investigations are focused on the accurate designing of CAR T-cells with clustered regularly interspaced short palindromic repeats(CRISPR)/CRISPR-associated protein 9(Cas9)system or other novel gene editing tools that can induce hereditary changes with or without the presence of a double-stranded break into the genome.These methodologies can be specifically focused on negative controllers of T-cells,induce modifications to a particular gene,and produce reproducible,safe,and powerful allogeneic CAR T-cells for on-demand cancer immunotherapy.The improvement of the CRISPR/Cas9 innovation offers an adaptable and proficient gene-editing capability in activating different pathways to help natural killer cells interact with novel CARs to particularly target tumor cells.Novel achievements and future challenges of combining next-generation CRISPR-Cas9 gene editing tools to optimize CAR T-cell and natural killer cell treatment for future clinical trials toward the foundation of modern cancer treatments have been assessed inthis review.

关键词： Cancer CAR T-cell CRISPR Gene editing Immunotherapy NK cell

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IRE1α regulates the PTHrP-IHH feedback loop to orchestrate chondrocyte hypertrophy and cartilage mineralization

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Genes & Diseases 2024年第1期11卷 464-478页

作者： Mengtian Fan Nana Geng Xingyue Li Danyang Yin Yuyou Yang Rong Jiang Cheng Chen Naibo Feng Li Liang Xiaoli Li Fengtao Luo Huabing Qi Qiaoyan Tan Yangli Xie Fengjin Guo Laboratory of Developmental Biology Department of Cell Biology and GeneticsSchool of Basic Medical ScienceChongqing Medical UniversityChongqing 400016China Laboratory of stem cells and Tissue engineering School of Basic Medical ScienceChongqing Medical UniversityChongqing 400016China Department of Orthopedics The 1st Affiliated Hospital of Chongqing Medical UniversityChongqing 400016China Department of Wound Repair and Rehabilitation Medicine State Key Laboratory of TraumaBurns and Combined InjuryTrauma CenterResearch Institute of SurgeryDaping HospitalArmy Medical UniversityChongqing 400042China

Cartilage development is controlled by the highly synergistic proliferation and differentiation of growth plate chondrocytes,in which the Indian hedgehog(IHH)and parathyroid hormone-related protein-parathyroid hormone-1 receptor(PTHrP-PTH1R)feedback loop is crucial.The inositol-requiring enzyme 1a/X-box-binding protein-1 spliced(IRE1α/XBP1s)branch of the unfolded protein response(UPR)is essential for normal cartilage development.However,the precise role of ER stress effector IRE1α,encoded by endoplasmic reticulum to nucleus signaling 1(ERN1),in skeletal development remains unknown.Herein,we reported that loss of IRE1α accelerates chondrocyte hypertrophy and promotes endochondral bone growth.ERN1 acts as a negative regulator of chondrocyte proliferation and differentiation in postnatal growth plates.Its deficiency interrupted PTHrP/PTH1R and IHH homeostasis leading to impaired chondrocyte hypertrophy and differentiation.XBP1s,produced by p-IRE1α-mediated splicing,binds and up-regulates PTH1R and IHH,which coordinate cartilage development.Meanwhile,ER stress cannot be activated normally in ERN1-deficient chondrocytes.In conclusion,ERN1 deficiency accelerates chondrocyte hypertrophy and cartilage mineralization by impairing the homeostasis of the IHH and PTHrP/PTH1R feedback loop and ER stress.ERN1 may have a potential role as a new target for cartilage growth and maturation.

关键词： Cartilage development ER stress ERN1 IHH PTHrP/PTH1R

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Targeted DNA N^(6)-methyladenine editing by dCas9 fused to METTL4 in the lepidopteran model insect Bombyx mori

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Insect Science 2024年第2期31卷 646-650页

作者： Feng Chen Hao Guo Weiqun Lan Mingyi Zhou Wenjng Geng Guanwang Shen Ping Lin Qingyou Xia Ping Zhao Zhiqing Li Integrative Science center of Germplasm Creation in Western China(chongqing)Science City Biological Science Research CenterSouthwest UniversityChongqingChina chongqing Key Laboratory of Sericultural Science Chongqing Engineering and Technology Research Center for Novel Silk MaterialsSouthwest UniversityChongqingChina

Dear Editor,N^(6)-Methyladenine(6mA)DNA modification is an important epigenetic mechanism with roles in regulating gene expression,nucleosome positioning,DNA damage repair,and cell cycle progression(Heyn&Esteller,2015;Luo et al.,2015;Boulias&Greer,2022).Despite progress in understanding the biological functions of 6mA,the contribution of individual 6mA installations on site-specific target genes is largely unknown,and therefore deciphering the molecular mechanism of 6mA in target gene expression has been difficult.

关键词： adenine fused Bombyx

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A Novel Poly(3-hexylthiophene) Engineered Interface for Electrochemical Monitoring of Ascorbic Acid During the Occurrence of Glutamate-Induced Brain Cytotoxic Edemas

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research 2024年第1期2023卷 301-313页

作者： Zexuan Meng Yuchan Zhang Lu Yang Shuang Zhao Qiang Zhou Jiajia Chen Jiuxi Sui Jian Wang Lizhong Guo Luyue Chang Jialing He Guixue Wang Guangchao Zang Institute of Life Science and Laboratory of Tissue and Cell BiologyLab Teaching and Management CenterChongqing Medical UniversityChongqing 400016China Key Laboratory for Biorheological Science and technology of Ministry of Education State and Local Joint Engineering Laboratory for Vascular ImplantsBioengineering College of Chongqing UniversityChongqing 400030China Jinfeng Laboratory Chongqing 401329China Department of Pathophysiology Chongqing Medical UniversityChongqingChina

Although neuroelectrochemical sensing technology offers unique benefits for neuroscience research,its application is limited by substantial interference in complex brain environments while ensuring biosafety requirements.In this study,we introduced poly(3-hexylthiophene)(P3HT)and nitrogen-doped multiwalled carbon nanotubes(N-MWCNTs)to construct a composite membrane-modified carbon fiber microelectrode(CFME/P3HT-N-MWCNTs)for ascorbic acid(AA)detection.The microelectrode presented good linearity,selectivity,stability,antifouling,and biocompatibility and exhibited great performance for application in neuroelectrochemical sensing.Subsequently,we applied CFME/P3HT-N-MWCNTs to monitor AA release from in vitro nerve cells,ex vivo brain slices,and in vivo living rat brains and determined that glutamate can induce cell edema and AA release.We also found that glutamate activated the N-methyl-d-aspartic acid receptor,which enhanced Na^(+) and Cl^(−) inflow to induce osmotic stress,resulting in cytotoxic edema and ultimately AA release.This study is the first to observe the process of glutamate-induced brain cytotoxic edema with AA release and to reveal the mechanism.Our work can benefit the application of P3HT in in vivo implant microelectrode construction to monitor neurochemicals,understand the molecular basis of nervous system diseases,and discover certain biomarkers of brain diseases.

关键词： release microelectrode Engine

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X-box binding protein 1 caused an imbalance in pyroptosis and mitophagy in immature rats with di-(2-ethylhexyl)phthalate-induced testis toxicity

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Genes & Diseases 2024年第2期11卷 935-951页

作者： Yifan Hong Xiazhu Zhou Qi Li Jing Chen Yuexin Wei Chunlan Long Lianju Shen Xiangqin Zheng Dinggang Li Xia Wang Chenjun Yu Shengde Wu Guanghui Wei Department of Urology Children's Hospital of Chongqing Medical UniversityChongqing 400014China Pediatric research Institute Children's Hospital of Chongqing Medical UniversityChongqing 400014China chongqing Key Laboratory of Children Urogenital Development and Tissue engineering Children's Hospital of Chongqing Medical UniversityChongqing 400014China chongqing Key Laboratory of Pediatrics Children's Hospital of Chongqing Medical UniversityChongqing 400014China Ministry of Education Key Laboratory of Child Development and Disorders Children's Hospital of Chongqing Medical UniversityChongqing 400014China National Clinical research center for Child Health and Disorders Children's Hospital of Chongqing Medical UniversityChongqing 400014China China International Science and technology Cooperation Base of Child Development and Critical Disorders Children's Hospital of Chongqing Medical UniversityChongqing 400014China

As a widely used plasticizer,di-(2-ethylhexyl)phthalate(DEHP)is known to induce significant testicular injury.However,the potential mechanism and effects of pubertal exposure to DEHP on testis development remain unclear.In vivo,postnatal day(PND)21 male rats were gavaged with 0,250,and 500 mg/kg DEHP for ten days.Damage to the seminiferous epithelium and disturbed spermatogenesis were observed after DEHP exposure.Meanwhile,oxidative stress-induced injury and pyroptosis were activated.Both endoplasmic reticulum(ER)stress and mitophagy were involved in this process.Monoethylhexyl phthalate(MEHP)was used as the biometabolite of DEHP in vitro.The GC-1 and GC-2 cell lines were exposed to 0,100μM,200μM,and 400μM MEHP for 24 h.Reactive oxygen species(ROS)generation,oxidative stress damage,ER stress,mitophagy,and pyroptosis were significantly increased after MEHP exposure.The ultrastructure of the ER and mitochondria was destroyed.X-box binding protein 1(XBP1)was observed to be activated and translocated into the nucleus.ROS generation was inhibited by acetylcysteine.The levels of antioxidative stress,ER stress,mitophagy,and pyroptosis were decreased as well.After the administration of the ER stress inhibitor 4-phenyl-butyric acid,both mitophagy and pyroptosis were inhibited.Toyocamycin-induced XBP1 down-regulation decreased the levels of mitophagy and pyroptosis.The equilibrium between pyroptosis and mitophagy was disturbed by XBP1 accumulation.In summary,our findings confirmed that DEHP induced a ROS-mediated imbalance in pyroptosis and mitophagy in immature rat testes via XBP1.Moreover,XBP1 might be the key target in DEHP-related testis dysfunction.

关键词： DEHP Mitophagy Pyroptosis Testicular development XBP1

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Recent advances of mechanosensitive genes in vascular endothelial cells for the formation and treatment of atherosclerosis

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Genes & Diseases 2024年第3期11卷 206-219页

作者： Shuyu Li Zichen Xu Yi Wang Lizhao Chen Xiangxiu Wang Yanghao Zhou Daoxi Lei Guangchao Zang Guixue Wang Key Laboratory of Biorheological Science and technology of Ministry of Education National and Local Joint Engineering Laboratory for Vascular ImplantsBioengineering College of Chongqing UniversityChongqing 400030China College of Basic Medical Sciences Chongqing Medical UniversityChongqing 400016China Department of Neurosurgery Daping HospitalArmy Medical Center of PLAArmy Medical UniversityChongqing 400042China

Atherosclerotic cardiovascular disease and its complications are a high-incidence disease worldwide.Numerous studies have shown that blood flow shear has a huge impact on the function of vascular endothelial cells,and it plays an important role in gene regulation of pro-inflammatory,pro-thrombotic,pro-oxidative stress,and cell permeability.Many impor-tant endothelial cell mechanosensitive genes have been discovered,including KLK10,CCN gene family,NRP2,YAP,TAZ,HIF-1α,NF-kB,FOS,JUN,TFEB,KLF2/KLF4,NRF2,and ID1.Some of them have been intensively studied,whereas the relevant regulatory mechanism of other genes remains unclear.Focusing on these mechanosensitive genes will provide new strategies for therapeutic intervention in atherosclerotic vascular disease.Thus,this article reviews the mechanosensitive genes affecting vascular endothelial cells,including classical pathways and some newly screened genes,and summarizes the latest research progress on their roles in the pathogenesis of atherosclerosis to reveal effective therapeutic targets of drugs and provide new insights foranti-atherosclerosis.

关键词： Atherosclerosis Blood flow Endothelial cell Mechanosensitive gene Therapeutic target

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Let-7i-5p maintains the stemness via R-spondin2/Wnt pathway in hepatocellular carcinoma

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Genes & Diseases 2024年第4期11卷 20-23页

作者： Qinghua Wei Xueshan Dai Jiahui Wei Wenwei Sun Xiaoqian Yang Yuxin Zhang Xin Guo Yi Chen College of Pharmaceutical Sciences&Chinese Medicine Southwest UniversityChongqing 400716China center for Basic Medical research TEDA International Cardiovascular HospitalChinese Academy of Medical Sciences&Peking Union Medical CollegeTianjin 300457China chongqing Key Laboratory of New Drug Screening from Traditional Chinese Medicine Chongqing 400716China pharmacology of Chinese Materia Medica-the Key Discipline Constructed by the State Administration of Traditional Chinese Medicine Chongqing 400716China Division of cell Developmental and Integrative BiologySchool of MedicineSouth China University of TechnologyGuangzhouGuangdong 510006China National Demonstration center for Experimental Pharmacy Education(Southwest University) Chongqing 400716China engineering research center of Coptis Development and Utilization(Ministry of Education) College of Pharmaceutical Sciences and Chinese MedicineSouthwest UniversityChongqing 400716China

Cancer stem cells(CSCs)are related to tumorigenesis,recurrence,metastasis,and drug resistance in hepatocellular carcinoma(HCC).1 Let-7i is a noncoding small RNA,belonging to the famous miRNA let-7 family.Recently,let-... 详细信息

关键词： hepatocellular Cancer metastasis

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