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The regulatory role of ZFAS1/mirnas/mrnas axis in cancer:a systematic review

Oncology Research 2025年第3期33卷 591-604页

作者： RAHUL KUMAR SINGH SUROJIT MANDAL ADRIJA MOHANTA RITU YADAV RAJIV RANJAN KUMAR RINKU KHATKAR VIVEK UTTAM UTTAM SHARMA MANJIT KAUR RANA MANJU JAIN HARDEEP SINGH TULI AKLANK JAIN Non-Coding RNA and Cancer Biology Laboratory Department of ZoologyCentral University of PunjabGhuddaBathinda151401India Department of Pathology/Lab Medicine All India Institute of Medical SciencesBathinda151001India Department of Biochemistry Central University of PunjabGhuddaBathinda151401India Department of Biotechnology Maharishi Markandeshwar(Deemed to be University)MullanaAmbala133207India

Objectives:Recently,we and others have demonstrated the involvement of Zinc Finger Antisense 1(ZFAS1)in cancer ***,the intricate interplay of ZFAS1 with mirnas and mrnas remains to be fully *** and methods:We followed PRISMA guidelines to retrieve and assess the available literature on the topic“ZFAS1/mirna/mrna axis”and“Cancer”from databases such as PubMed,Google Scholar,and *** also used bioinformatic webtools for analyzing the potential mirna targets of ZFAS1 and its role in survival of cancer patients along with their role in various biological functions and ***:Our literature search and bioinformatic analysis reveals that ZFAS1 serves as a sponge for numerous *** the various targeted mirnas,miR-150-5p stands out as significantly correlated with ZFAS1 across multiple databases(p-value=3.27e-16,R-value=-0.346).Additionally,our Kaplan-Meier survival analysis indicates a noteworthy association between ZFAS1 expression levels and overall poor prognosis and survival rates in ovarian,sarcoma,and pancreatic *** also underscore the involvement of various signaling pathways,including Signal Transducer and Activator of Transcription 3(STAT3),Spindle and Kinetochore-associated Protein 1(SKA1),Lysophosphatidic acid receptor 1(LPAR1),and Wntβ-catenin,in cancer development through the ZFAS1/mirnas/mrnas ***,we identify ZFAS1’s pivotal roles in diverse molecular processes,such as rna binding and ribonucleoprotein ***:In conclusion,this review comprehensively summarizes the latest advancements in understanding the regulatory relationships among ZFAS1,mirnas,and mrnas,emphasizing their collective role in cancer development to propose innovative avenues for cancer *** believe that the intricate relationship among the ZFAS1-mirna-mrna axis may yield potential therapeutic targets for effective cancer management.

关键词： Lncrna mirna mrnas Zinc finger antisense 1(ZFAS1) Cancer biomarker

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Platelet-rich plasma-derived exosomes accelerate the healing of diabetic foot ulcers by promoting macrophage polarization toward the M2 phenotype

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Clinical and Experimental Medicine 2025年第1期25卷 1-13页

作者： He, Ling Zhao, Nan Chen, Xiaoling Zhang, Wenjie Lv, Kun Xu, Yuanhong Department of Clinical Laboratory The First Affiliated Hospital of Anhui Medical University Anhui Hefei 230000 China Key Laboratory of Non-Coding RNA Transformation Research of Anhui Higher Education Institution (Wannan Medical College) Anhui Wuhu 241001 China Blood transfusion department of Yijishan Hospital The First Affiliated Hospital of Wannan Medical College Anhui Wuhu 241001 China Academy of Laboratory Medicine Wannan Medical College Anhui Wuhu 241001 China Central Laboratory Yijishan Hospital The First Affiliated Hospital of Wannan Medical College Anhui Wuhu 241001 China

Diabetic foot ulcers (DFUs) impose a significant clinical and socioeconomic burden on patients and healthcare systems. Although platelet-rich plasma (PRP) and platelet-rich plasma-derived exosomes (PRP-Exos) have emerged as promising therapeutic agents in tissue regeneration, the mechanisms underlying the immunomodulatory effects of PRP and PRP-Exos—particularly their role in macrophage polarization—remain poorly understood. In this study, we isolated and characterized PRP-Exos and systematically evaluated their therapeutic potential in diabetic wound healing via comprehensive in vivo and in vitro experiments. Our results revealed that both PRP-gel and PRP-Exos significantly enhanced diabetic wound healing by promoting macrophage polarization toward the anti-inflammatory M2 phenotype. These findings suggest that PRP-Exos represent a novel and effective therapeutic strategy for DFUs, providing a robust rationale for future clinical translation. © The Author(s) 2025.

关键词： Diabetic foot ulcers M2 Macrophage polarization Platelet-rich plasma Platelet-rich plasma-derived exosomes

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Rosaceae phylogenomic studies provide insights into the evolution of new genes

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Horticultural Plant Journal 2025年第1期11卷 389-405页

作者： Lan Jiang Xiaoxu Li Kun Lyu Han Wang Zhiyuan Li Wang Qi Lin Zhang Yunpeng Cao Anhui Province Key Laboratory of Non-coding RNA Basic and Clinical Transformation(Wannan Medical College) Central LaboratoryYijishan Hospital of Wannan Medical CollegeWuhuAnhui 241000China Beijing Life Science Academy Beijing 102209China CAS Key Laboratory of Plant Germplasm Enhancement and Specialty Agriculture Wuhan Botanical GardenChinese Academy of SciencesWuhanHubei 430074China Center of Economic Botany Core Botanical GardensChinese Academy of SciencesWuhanHubei 430074China Key Laboratory for Tobacco Gene Resources Tobacco Research InstituteChinese Academy of Agricultural SciencesQingdaoShangdong 266000China school of Life Sciences Anhui Agricultural UniversityHefeiAnhui 230036China School of Basic Medical Sciences Hubei University of Chinese MedicineWuhanHubei 430065China

Rosa banksiae,known as Lady Banks'rose,is a perennial ornamental crop and a versatile herb in traditional Chinese *** the lack of genomic resources,we assembled a Hi Fi and Nanopore sequencing-derived 458.58 Mb gap-free telomere-to-telomere high-quality *** genome with a scaffold N50=63.90 *** genome of *** exhibited no lineage-specific whole-genome duplication compared with other *** phylogenomic analysis of 13 Rosaceae and Arabidopsis through a comparative genomics study showed that numerous gene families were lineage-specific both before and after the diversification of *** of these genes are candidates for new genes that have evolved from parental genes through fusion *** genes are divided into three types:Type-I and Type-II genes contain two parental genes that are generated by duplication,distributed in the same and different regions of the genome,respectively;and Type-III can only be detected in one parental ***,Type-I genes are found to have more relaxed selection pressure and lower Ks values than Type-II,indicating that these newly evolved Type-I genes may play important roles in driving phenotypic *** analysis exhibited that newly formed fusion genes can regulate the phenotype traits of plant growth and development,suggesting the functional significance of these *** study identifies new fusion genes that could be responsible for phenotype evolution and provides information on the evolutionary history of recently diverged species in the Rosa *** data represents the major progress in understanding the new fusion genes evolution pattern of Rosaceae and provides an invaluable resource for phylogenomic studies in plants.

关键词： Rosa banksiae Gap-free genome Rosaceae Phenotype Evolutionary patterns

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Carnitine palmitoyltransferase 1C promotes EMT-associated cisplatin resistance in non-small cell lung cancer cells

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Cancer Biology & Medicine 2025年第1期22卷 48-66页

作者： Renjie Chen Jiahui Wang Shuoyu Huang Xuefeng Hu Xinran He Tiange Zhang Yunhan Hu Huijun Wei Sihui Nian Yushu Huang Zhihao Wu Research Laboratory of Tumor Microenvironment Wannan Medical CollegeWuhu 241001China School of Laboratory Medicine Wannan Medical CollegeWuhu 241001China School of Anesthesiology Wannan Medical CollegeWuhu 241001China School of Medical Imageology Wannan Medical CollegeWuhu 241001China School of Clinical Medicine Wannan Medical CollegeWuhu 241001China Anhui Province Key Laboratory of Active Biological Macro-molecules Research Wannan Medical CollegeWuhu 241001China Provincial Engineering Laboratory for Screening and Re-evaluation of Active Compounds of Herbal Medicines in Southern Anhui Wannan Medical CollegeWuhu 241001China School of Pharmacy Wannan Medical CollegeWuhu 241001China Anhui Province Key Laboratory of Non-coding RNA Basic and Clinical Transformation Wannan Medical CollegeWuhu 241001China Anhui Provincial Engineering Research Center for Dental Materials and Application Wannan Medical CollegeWuhu 241001China

Objective:Lung cancer is the most common cause of cancer-related deaths ***-based chemotherapy is one of the main treatment options for patients with non-small cell lung cancer(NSCLC)but the effectiveness of chemotherapy is encumbered by drug ***,understanding the molecular mechanisms underlying chemotherapy resistance is crucial in improving treatment outcomes and ***:The cell viability assay and apoptosis were used to analyze *** blot analysis and wound healing testing were used to evaluate the epithelial-to-mesenchymal transition(EMT).Immunoprecipitation was used for analysis of protein *** activity was determined using the luciferase reporter *** staining was used to determine reactive oxygen species *** expression patterns of EMT markers and carnitine palmitoyltransferase 1C(CPT1C)were determined by Western blot ***:CPT1C,which was shown to be highly expressed in lung cancer,is associated with cisplatin resistance in NSCLC ***1C depletion increased NSCLC cell sensitivity to cisplatin,while overexpression of CPT1C increased NSCLC cell resistance to *** of EMT mediated CPT1C-induced cisplatin *** expression of Snail reversed the increase in cisplatin sensitivity triggered by CPT1C ***,CPT1C was shown to be regulated at the post-translational level and an E3-ubiquitin ligase,NEDD4L,was shown to be a major regulator of CPT1C stability and ***:These data provide evidence for the first time that the lipid metabolism enzyme,CPT1C,mediates resistance to ***,the use of combination therapy with a CPT1C inhibitor may be a promising new avenue in lung cancer treatment.

关键词： CPT1C chemoresistance EMT NEDD4L NSCLC

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Disulfidptosis in tumor progression

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Cell Death Discovery 2025年第1期11卷 1-16页

作者： Wan, Senlin Liang, Changming Wu, Chengwei Wang, Song Wang, Jiawei Xu, Lishuai Zhang, Xu Hou, Yinfen Xia, Yabin Xu, Li Huang, Xiaoxu Department of Gastrointestinal Surgery The First Affiliated Hospital Yijishan Hospital of Wannan Medical College Anhui Wuhu China Anhui Province Key Laboratory of Non-coding RNA Basic and Clinical Transformation Anhui Wuhu China

Disulfidptosis, a regulated cell death modality driven by the cystine transporter solute carrier family 7 member 11 (SLC7A11), is characterized by actin cytoskeleton collapse under glucose starvation. This review systematically elucidates the pivotal role of disulfidptosis in tumor metabolic reprogramming, with a focus on its molecular mechanisms and distinctions from other cell death pathways. The core mechanisms include SLC7A11-mediated cystine overload and NRF2/c-Myc-regulated pentose phosphate pathway activation. By integrating multiomics data and single-cell transcriptomics, we comprehensively decipher the heterogeneous expression patterns of disulfidptosis-related genes (DRGs) and their dynamic interplay with immune microenvironment remodeling. Furthermore, the coexpression networks of DRGs and disulfidptosis-related long noncoding rnas (DRLs) offer novel insights into tumor diagnosis, prognosis, and targeted therapy. Therapeutically, SLC7A11 inhibitors (e.g., HG106) and glucose transporter inhibitors (e.g., BAY-876) demonstrate efficacy by exploiting metabolic vulnerabilities, whereas natural compounds synergizing with immune checkpoint blockade provide strategies to counteract immunosuppressive microenvironments. Through interdisciplinary collaboration and clinical translation, disulfidptosis research holds transformative potential in redefining precision oncology. © The Author(s) 2025.

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Transposon–host arms race: a saga of genome evolution

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Trends in Genetics 2025年第5期41卷 369-389页

作者： Iwasaki, Yuka W. Shoji, Keisuke Nakagwa, Shinichi Miyoshi, Tomoichiro Tomari, Yukihide Laboratory for Functional Non-coding Genomics RIKEN Center for Integrative Medical Sciences 1-7-22 Suehiro-cho Tsurumi-ku Kanagawa Yokohama 230-0045 Japan of Bio-Applications and Systems Engineering Tokyo University of Agriculture and Technology Tokyo Koganei-shi 184-8588 Japan Laboratory of RNA Function Institute for Quantitative Biosciences The University of Tokyo 1-1-1 Yayoi Tokyo Bunkyo-ku 113-0032 Japan RNA Biology Laboratory Faculty of Pharmaceutical Sciences Hokkaido University Kita 12-jo Nishi 6-chome Kita-ku Sapporo 060-0812 Japan Laboratory for Retrotransposon Dynamics RIKEN Center for Integrative Medical Sciences 1-7-22 Suehiro-cho Tsurumi-ku Kanagawa Yokohama 230-0045 Japan Department of Computational Biology and Medical Sciences of Frontier Sciences The University of Tokyo Tokyo Bunkyo-ku 113-0032 Japan

Once considered ‘junk DNA,’ transposons or transposable elements (TEs) are now recognized as key drivers of genome evolution, contributing to genetic diversity, gene regulation, and species diversification. However, their ability to move within the genome poses a potential threat to genome integrity, promoting the evolution of robust host defense systems such as Krüppel-associated box (KRAB) domain-containing zinc finger proteins (KRAB-ZFPs), the human silencing hub (HUSH) complex, 4.5SH rnas, and PIWI-interacting rnas (pirnas). This ongoing evolutionary arms race between TEs and host defenses continuously reshapes genome architecture and function. This review outlines various host defense mechanisms and explores the dynamic coevolution of TEs and host defenses in animals, highlighting how the defense mechanisms not only safeguard the host genomes but also drive genetic innovation through the arms race. © 2025 Elsevier Ltd

关键词： evolutionary arms race genetic conflicts genome evolution host defense mechanisms transposable elements (TEs)

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Inhibition of KDM6B prevents osteoarthritis by blocking growth plate-like H3K27me3 loss in bivalent genes

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Science China Life Sciences 2025年第5期68卷 1423-1436页

作者： Hao Du Yao Zhang Xi Yu Xuanhe You Diwei Wu Ze Du Yongrui Cai Zhenyu Luo Hanpeng Lu Zhixin Liao Bi-Sen Ding Ya Zhao Yan Wang Ke Xiao Fan Yang Fangji Gan Ning Ning Jiancheng Zeng Peiliang Shi Zongke Zhou Shishu Huang Department of Orthopedic Surgery and Orthopedic Research Institute West China HospitalSichuan University Rehabilitation Medicine Center West China HospitalSichuan University Key Laboratory of Birth Defects and Related Diseases of Women and Children of MOE State Key Laboratory of BiotherapyWest China Second University HospitalSichuan University Institute of Translational Medicine Medical CollegeYangzhou University Jiangsu Key Laboratory of Experimental & Translational Non-coding RNA Research College of Animal Science and Technology Sichuan Agricultural University Farm Animal Genetic Resources Exploration and Innovation Key Laboratory of Sichuan Province Sichuan Agricultural University Department of Lower Limb Surgery of Sichuan Province Orthopedic Hospital Central Laboratory of Sichuan Province Orthopedic Hospital Brain Cognition and Brain Disease Institute (BCBDI) Shenzhen Institute of Advanced TechnologyChinese Academy of Sciences (CAS)Shenzhen-Hong Kong Institute of Brain Science-Shenzhen Fundamental Research Institutions School of Mechanical Engineering Sichuan University Gem Pharmatech (Chengdu) Co. Ltd.

Osteoarthritis(OA) is the most prevalent joint disorder occurring with articular cartilage degradation. It includes a switch from an articular to a growth plate chondrocyte phenotype. Here, we investigated the histone modification profiles and found significant H3K27me3 loss in OA, which led to disease-associated gene expression. Surprisingly, these genes were occupied by both H3K27me3 and H3K4me3 in normal chondrocytes, showing a poised bivalent state. Furthermore, we observed the derepression of similar bivalent genes in growth plate chondrocytes. Finally, a KDM6B inhibitor GSK-J4 prevented the H3K27me3 loss and cartilage damage in the rat OA model. Our results reveal an inherited bivalent epigenetic signature on developmental genes that makes articular chondrocytes prone to hypertrophy and contributes to a promising epigenetic therapy for OA.

关键词： osteoarthritis histone modifications H3K27me3 bivalency growth plate

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Crystal structure of E. coli arginyl-trna synthetase and ligand binding studies revealed key residues in arginine recognition

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Protein & Cell 2014年第2期5卷 151-159页

作者： Kelei Bi Yueting Zheng Feng G"ao Jianshu Dong Jiangyun Wang Yi Wang Weimin Gong Laboratory of Non-coding RNA Institute of Biophysics Chinese Academy of Sciences

The arginyl-trna synthetase(ArgRS) catalyzes the esterification reaction between L-arginine and its cognate trnaArg. Previously reported structures of ArgRS shed considerable light on the trna recognition mechanism, while the aspect of amino acid binding in ArgRS remains largely unexplored. Here we report the first crystal structure of E. coli ArgRS(eArgRS) complexed with L-arginine, and a series of mutational studies using isothermal titration calorimetry(ITC). Combined with previously reported work on ArgRS, our results elucidated the structural and functional roles of a series of important residues in the active site, which furthered our understanding of this unique enzyme.

关键词： arginyl-trna synthetase amino acyl-trna synthetase isothermal titration calorimetry site-directed mutation X-ray crystal structure E. coli

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A genetically encoded sulfotyrosine for VHR function research

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Protein & Cell 2013年第10期4卷 731-734页

作者： Yueting Zheng Xiaoxuan Lv Jiangyun Wang Laboratory of Non-coding RNA Institute of BiophysicsChinese Academy of SciencesBeijing 100101China

Dear Editor,Protein tyrosine phosphorylation is one of the most prevalent forms of post-translational modification and plays a signifi cant role in the control of a variety of cellular processes,including signal transduction,and is implicated in many human diseases(Eckhart et al.,1979;Karisch et al.,2011).The human vac-cinia H1-related phosphatase(VHR),the fi rst human dual specifi city protein phos-phatase(DSP),hydrolyzes phosphate monoesters from phosphotyrosine,phosphothreonine,or phosphoserine residues(Aroca et al.,1995).DSPs func-tion in signal transduction and in control of the cell cycle;more than 20 mamma-lian DSPs have so far been identifi *** VHR can dephosphorylate both Erk and Jnk in vivo(Schumacher et al.,2002),it differs from other‘typi-cal’mitogen activated protein(MAP)kinase phosphatases(MKPs).With only 185 amino acids,VHR consists of only a catalytic domain with no recogniz-ing or docking domain.

关键词： al. diseases ed.

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Ginsenoside Rg5 alleviates radiation-induced acute lung vascular endothelium injury by reducing mitochondrial apoptosis via Sirt1

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Journal of Ginseng Research 2025年第3期49卷 260-270页

作者： Li, Churong Zhao, Biao Xiong, Jing Li, Linjie Pang, Dalong Unger, Keith Jung, Mira Lyu, Jiahua Kuang, Hao Liang, Long Li, Tao Chen, Long Bai, Hansong Radiotherapy Center Radiation Oncology Key Laboratory of Sichuan Province Sichuan Clinical Research Center for Cancer Sichuan Cancer Hospital & Institute Sichuan Cancer Center University of Electronic Science and Technology of China Chengdu China Non-Coding RNA and Drug Discovery Key Laboratory of Sichuan Province School of Basic Medical Sciences Chengdu Medical College Chengdu China Department of Integrative Chinese and Western Medicine Sichuan Cancer Hospital & Institute Sichuan Cancer Center Affiliated Cancer Hospital of the University of Electronic Science and Technology of China Chengdu China Department of Immunology School of Basic Medical Sciences Chengdu Medical College Chengdu China Department of Radiation Medicine Lombardi Comprehensive Cancer Center Georgetown University Medical Center Washington DC United States Department of Oncology The Affiliated Hospital of Southwest Medical University Luzhou China School of Medicine University of Electronic Science and Technology of China Chengdu China

Background: Ginsenoside Rg5 possesses potent anti-oxidative, anti-inflammatory, and cytoprotective properties. This study explored the protective effects of ginsenoside Rg5 on radiation-induced pulmonary microvascular endothelial cells (PMECs) injury and the associated molecular mechanisms. Materials and methods: C57BL/6 mice were used for in vivo studies and primary human PMECs (PPMECs) were utilized as in vitro models. Mice with or without ginsenoside Rg5 pretreatment were irradiated by varying doses. Lung tissues were analyzed for histopathological changes and the expression of endothelial markers. In vitro, PPMECs were irradiated with or without ginsenoside Rg5 pretreatment and analyzed for apoptosis, oxidative stress, mitochondrial function, and endothelial barrier integrity. Results: Ginsenoside Rg5 pretreatment attenuated radiation-induced acute lung damage, preserved endothelial cell junction integrity, and maintained endothelial barrier function in vivo. In vitro, ginsenoside Rg5 significantly reduced IR-induced oxidative stress, apoptosis, and mitochondrial dysfunction in PPMECs. Ginsenoside Rg5 suppressed radiation-induced Mfn2 acetylation and proteasomal degradation via Sirt1-mediated deacetylation, thereby preserving mitochondrial dynamics and integrity. The protective effects of ginsenoside Rg5 on the integrity of mitochondrial and endothelial tight junction proteins and barrier function were also Sirt1-dependent. Conclusions: Ginsenoside Rg5 exerts a protective effect against radiation-induced endothelial injury by modulating mitochondrial dynamics and function, as well as maintaining endothelial barrier integrity, in a Sirt1-dependent manner. © 2025

关键词： Endothelial cell injury Ginsenoside Rg5 Mitochondrial dynamics Radiation Sirt1

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