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Construction and validation of somatic mutation-derived long noncoding RNAs signatures of Genomic instability to predict prognosis of hepatocellular carcinoma

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World Journal of Gastrointestinal Surgery 2024年第3期16卷 842-859页

作者： Bo-Tao Duan Xue-Kai Zhao Yang-Yang Cui De-Zheng Liu Lin Wang Lei Zhou Xing-Yuan Zhang Department of Hepatobiliary Surgery Binzhou Medical University HospitalBinzhou 256600Shandong ProvinceChina Department of Ophthalmology Binzhou Medical University HospitalBinzhou 256600Shandong ProvinceChina

BACKGROUND Long non-coding RNAs(LncRNAs)have been found to be a potential prognostic factor for cancers,including hepatocellular carcinoma(HCC).Some LncRNAs have been confirmed as potential indicators to quantify Genomic instability(GI).Nevertheless,GI-LncRNAs remain largely unexplored.This study established a GI-derived LncRNA signature(GILncSig)that can predict the prognosis of HCC patients.AIM To establish a GILncSig that can predict the prognosis of HCC patients.METHODS Identification of GI-LncRNAs was conducted by combining LncRNA expression and somatic mutation profiles.The GI-LncRNAs were then analyzed for functional enrichment.The GILncSig was established in the training set by Cox regression analysis,and its predictive ability was verified in the testing set and TCGA set.In addition,we explored the effects of the GILncSig and TP53 on prognosis.RESULTS A total of 88 GI-LncRNAs were found,and functional enrichment analysis showed that their functions were mainly involved in small molecule metabolism and GI.The GILncSig was constructed by 5 LncRNAs(miR210HG,AC016735.1,AC116351.1,AC010643.1,LUCAT1).In the training set,the prognosis of high-risk patients was significantly worse than that of low-risk patients,and similar results were verified in the testing set and TCGA set.Multivariate Cox regression analysis and stratified analysis confirmed that the GILncSig could be used as an independent prognostic factor.Receiver operating characteristic curve analysis of the GILncSig showed that the area under the curve(0.773)was higher than the two LncRNA signatures published recently.Furthermore,the GILncSig may have a better predictive performance than TP53 mutation status alone.CONCLUSION We established a GILncSig that can predict the prognosis of HCC patients,which will help to guide prognostic evaluation and treatment decisions.

关键词： Genomic instability Long noncoding RNA Hepatocellular carcinoma Prognosis Diagnosis

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Genomic instability and eye diseases

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Advances in Ophthalmology Practice and Research 2023年第3期3卷 103-111页

作者： Hongyan Liu Jun Cheng Xiaoyun Zhuang Benxiang Qi Fenfen Li Bining Zhang Eye Institute of Shandong First Medical University Qingdao Eye Hospital of Shandong First Medical UniversityQingdaoChina School of Ophthalmology Shandong First Medical UniversityQingdaoChina State Key Laboratory Cultivation Base Shandong Provincial Key Laboratory of OphthalmologyQingdaoChina Eye Institute of Shandong First Medical University Eye Hospital of Shandong First Medical University(Shandong Eye Hospital)JinanChina Department of Ophthalmology School of Clinical MedicineWeifang Medical UniversityWeifangChina The Eye Hospital of Wenzhou Medical University HangzhouChina

Background:Genetic information is stored in the bases of double-stranded DNA.However,the integrity of DNA molecules is constantly threatened by various mutagenic agents,including pollutants,ultraviolet light(UV),and medications.To counteract these environmental damages,cells have established multiple mechanisms,such as producing molecules to identify and eliminate damaged DNA,as well as reconstruct the original DNA structures.Failure or insufficiency of these mechanisms can cause genetic instability.However,the role of genome stability in eye diseases is still under-researched,despite extensive study in cancer biology.Main text:As the eye is directly exposed to the external environment,the genetic materials of ocular cells are constantly under threat.Some of the proteins essential for DNA damage repair,such as pRb,p53,and RAD21,are also key during the ocular disease development.In this review,we discuss five ocular diseases that are associated with Genomic instability.Retinoblastoma and pterygium are linked to abnormal cell cycles.Fuchs’corneal endothelial dystrophy and age-related macular degeneration are related to the accumulation of DNA damage caused by oxidative damage and UV.The mutation of the subunit of the cohesin complex during eye development is linked to sclerocornea.Conclusions:Failure of DNA damage detection or repair leads to increased Genomic instability.Deciphering the role of Genomic instability in ocular diseases can lead to the development of new treatments and strategies,such as protecting vulnerable cells from risk factors or intensifying damage to unwanted cells.

关键词： Genomic instability Ocular diseases Retinoblastoma Cornea Pterygium

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Cellular exposure to muscle relaxants and propofol could lead to Genomic instabilityin vitro

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The Journal of Biomedical Research 2012年第2期26卷 117-124页

作者： Allen Edward Coleman Nicole McNeil Alexander Leonidovich Kovalchuck Dara Wangsa Thomas Ried Hong Wang Department of Anesthesiology Wayne State UniversityDetroit Medical CenterDetroitMichigan 48201USA Laboratory of Cancer genomics National Cancer InstituteNational Institutes of HealthBethesdaMaryland 20892USA Laboratory of Immunogenetics National Institute of Allergy and Infectious DiseaseNational Institutes of HealthRockvilleMaryland 20852USA

Anesthesia is widely used in several medical settings and accepted as safe. However, there is some evidence that anesthetic agents can induce genomic changes leading to neural degeneration or apoptosis. Although chromosomal changes have not been observed in vivo, this is most likely due to DNA repair mechanisms, apoptosis, or cellular senescence. Potential chromosomal alterations after exposure to common anesthetic agents may be relevant in patients with Genomic instability syndromes or with aggressive treatment of malignancies. In this study, the P388 murine B cells were cultured in vitro, and spectral karyotyping （SKY） was utilized to uncover genomewide changes. Clinically relevant doses of cisatracurium and propofol increased structural and numerical chromosomal instability. These results may be relevant in patients with underlying chromosomal instability syndromes or concurrently being exposed to chemotherapeutic agents. Future studies may include utilization of stimulated peripheral blood lymphocytes to further confirm the significance of these results.

关键词： spectral karyotyping （SKY） Genomic instability epigenetic P388 propofol cisatracurium vecuronium pancuronium aneuploidy

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Genomic instability Is a Mechanism for Diminished Male Fertility Following Chronic Dichlorvos Exposure

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Journal of Biosciences and Medicines 2023年第7期11卷 37-49页

作者： Raymond A. Vhriterhire Samuel O. Odeh Gideon U. Egesie Department of Anatomical Pathology College of Health Sciences Benue State University Makurdi Nigeria Department of Human Physiology Faculty of Basic Medical Sciences College of Health Sciences University of Jos Jos Nigeria

Background and Objectives: Chronic low-dose exposure to dichlorvos occurs in communities in Africa where the substance is used indiscriminately for a variety of purposes. This experiment used an animal model to evaluate Genomic instability induced by this pattern of chronic exposure and its relationship with some measures of fertility in males. Methods: Seventy-five male Rattus norvegicus rats obtained for this experiment, were randomly allotted into five groups. Dichlorvos was given by oral gavage at doses of 0.28 mg/kg, 0.56 mg/kg and, 1.68 mg/kg, respectively, to three of the groups, on alternate days for 50 weeks. The remaining two groups received plain drinking water and cyclophosphamide as negative and positive controls, respectively. Samples were collected at 17, 34, and 50 weeks. Sperm count, sperm morphology and serum levels of follicle-stimulating hormone, luteinizing hormone, dihydrotestosterone, oestrogen and progesterone were determined. Furthermore, the frequency of micronucleated polychromatic erythrocytes was determined in bone marrow cells obtained from the femur. Results: The mean ranks of micronuclei frequency had an increasing trend. The frequency of micronucleated polychromatic erythrocytes (MnPCE) had a significant negative correlation with oestrogen (rs = -0.47, p = 0.00, n = 50), follicle-stimulating hormone (rs = -0.41, p = 0.00, n = 50) and progesterone (rs = -0.37, p = 0.01, n = 50) serum levels. A positive monotonic relationship also existed between micronuclei frequency and those of tubular necrosis, tubular vacuolation, and residual bodies. A positive significant moderate correlation was found between MnPCE and the proportion of immotile sperms (rs = 0.41, p = 0.00, n = 50). Conclusion: The nature of the correlations between micronuclei frequency and the proportion of immotile sperms, adverse histological changes and serum hormone levels found in this study suggest Genomic instability as the possible mechanism for diminished fertility in ma

关键词： Genomic instability Micronuclei Male Infertility Dichlorvos Chronic Organophosphate Exposure

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Genomic instability of telomere,telomerase,and their relationship with radiation carcinogenesis

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吉林大学学报(医学版) 1998年第5期 538-544页

作者： Cai Lu 1,Wang Guanjun 2 Cai Lu et al Genomic instability of telomere,telomerase,and their…(1 Institutes of Radiation Medicine,NBUMS & Department of Pathology,The Universtiy of Western Ontario,Canada 2 Department of Hematology,First Clinical Colle

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More efficient induction of genotoxicity by high-LET Fe-particle radiation than low-LET X-ray radiation at low doses

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Radiation Medicine and Protection 2023年第1期4卷 11-18页

作者： Bing Wang Takanori Katsube Kaoru Tanaka Yasuharu Ninomiya Hirokazu Hirakawa Cuihua Liu Kouichi Maruyama Masahiro Murakami Tetsuo Nakajima Akira Fujimori Mitsuru Nenoi National Institutes for Quantum Science and Technology Chiba263-8555Japan

Objective:To understand differential effects on induction of genotoxicity and Genomic instability(GI)by high-LET particle radiation and low-LET photon radiation,based on ground-based experiments using total body irradiation(TBI)of mice with Fe-particle radiation and X-ray radiation.Methods:TBI was delivered to C57BL/6J Jms strain female mice of 8 weeks old at a dose ranging from 0.1 to 3.0 Gy of Fe-particle radiation or at a dose ranging from 0.1 to 5.0 Gy of X-ray radiation.Induction of genotoxicity and GI by TBI was determined respectively at 1 and 2 months after exposure using frequency of micronuclei in bone marrow erythrocytes as the endpoint.Inhibition of bone marrow cell proliferation by TBI was measured as reduced erythropoiesis.Physiological conditions were also investigated.Results:TBI,regardless of the type of radiation,caused statistically significant increase in genotoxicity at 1 month after exposure,but did not induce GI at 2 months after exposure even at higher doses(>1.0 Gy).The doseresponse curve for the frequency of micronucleated polychromatic erythrocytes induced by Fe-particle radiation and X-ray radiation was y=0.7798 t 1.7889x–0.5978x^(2)(R^(2)=0.8109)and y=0.7421 t 1.3792x–0.2588 x^(2)(R^(2)=0.8081),respectively.The dose-response curve for the frequency of micronucleated normochromatic erythrocytes induced by Fe-particle radiation and X-ray radiation was y=0.7191 t 1.4545x–0.4978x^(2)(R^(2)=0.7047)and y=0.658 t 1.344x–0.2531x^(2)(R^(2)=0.7853),respectively.In general,high-LET Fe-particle radiation was more efficient in inducing genotoxicity than low-LET X-ray radiation at lower doses(<0.5 Gy).Conclusions:These results further confirm that exposure to TBI,even at higher doses and regardless the type of radiation,does not induce GI in C57BL/6J strain mice measured as increased micronuclei in bone marrow erythrocytes.These findings indicate that radiation-induced GI is mouse strain dependent and suggest that more comprehensive studies should be done to explore the late health consequences fro

关键词： Fe-particle radiation Genotoxicity Genomic instability Micronucleated erythrocyte C57BL/6J mice

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Alterations of DNA damage response pathway:Biomarker and therapeutic strategy for cancer immunotherapy

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Acta Pharmaceutica Sinica B 2021年第10期11卷 2983-2994页

作者： Minlin Jiang Keyi Jia Lei Wang Wei Li Bin Chen Yu Liu Hao Wang Sha Zhao Yayi He Caicun Zhou Department of Medical Oncology Shanghai Pulmonary HospitalTongji University Medical School Cancer InstituteTongji University School of MedicineShanghai 200433China Medical School Tongji UniversityShanghai 200433China

Genomic instability remains an enabling feature of cancer and promotes malignant transformation.Alterations of DNA damage response(DDR)pathways allow Genomic instability,generate neoantigens,upregulate the expression of programmed death ligand 1(PD-L1)and interact with signaling such as cyclic GMPe AMP synthase-stimulator of interferon genes(cGASe STING)signaling.Here,we review the basic knowledge of DDR pathways,mechanisms of Genomic instability induced by DDR alterations,impacts of DDR alterations on immune system,and the potential applications of DDR alterations as biomarkers and therapeutic targets in cancer immunotherapy.

关键词： DNA damage response DNA repair Immunotherapy Genomic instability Tumor microenvironment PD-1 PD-L1 cGASe STING

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Evolving insights:how DNA repair pathways impact cancer evolution

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Cancer Biology & Medicine 2020年第4期17卷 805-827页

作者： Jiadong Zhou Xiao Albert Zhou Ning Zhang Jiadong Wang Department of Radiation Medicine Institute of Systems BiomedicineSchool of Basic Medical SciencesPeking University Health Science CenterBeijing 100191China Biomedical Pioneering Irmovation Center(BIOPIC)and Translational Cancer Research Center School of Life SciencesFirst HospitalPeking UniversityBeijing 100871China Laboratory of Cancer Cell Biology Tianjin Medical University Cancer Instituteand HospitalNational Clinical Research Center for CancerKey Laboratory of Cancer Prevention and TherapyTianjinTianjin's Clinical Research Center for CancerTianjin 300060China

Viewing cancer as a large,evolving population of heterogeneous cells is a common perspective.Because Genomic instability is one of the fundamental features of cancer,this intrinsic tendency of genomic variation leads to striking intratumor heterogeneity and functions during the process of cancer formation,development,metastasis,and relapse.With the increased mutation rate and abundant diversity of the gene pool,this heterogeneity leads to cancer evolution,which is the major obstacle in the clinical treatment of cancer.Cells rely on the integrity of DNA repair machineries to maintain genomic stability,but these machineries often do not function properly in cancer cells.The deficiency of DNA repair could contribute to the generation of cancer Genomic instability,and ultimately promote cancer evolution.With the rapid advance of new technologies,such as single-cell sequencing in recent years,we have the opportunity to better understand the specific processes and mechanisms of cancer evolution,and让s relationship with DNA repair.Here,we review recent findings on how DNA repair affects cancer evolution,and discuss how these mechanisms provide the basis for critical clinical challenges and therapeutic applications.

关键词： DNA repair cancer evolution intratumor heterogeneity Genomic instability drug resistance

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Tumor growth and metastasis can be inhibited by maintaining genomic stability in cancer cells

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Frontiers of Medicine 2015年第1期9卷 57-62页

作者： Yi Liang Sun Yat-sen University Cancer Center State Key Laboratory of Oncology in South China ' Collaborative Innovation Center for CancerMedicine Department of Experimental Research Department of Medical Oncology Sun Yat-sen University Cancer Center Guangzhou 510060 China Department of Hepatobiliary Oncology Affiliated Tumor Hospital Guangzhou Medical University Guangzhou 510095 China Peking Union Medical College Chinese Academy of Medical Sciences Beijing 100730 China

The existence of cancer stem cells, stem-like cancer cells （SLCCs）, or tumor-initiating cells is considered as the cause of tumor formation and recurrence, indicating the importance of studying novel therapy that targets SLCCs. The origin of SLCCs is controversial because of two competing hypotheses： SLCCs are either transformed from tissue adult stem cells or dedifferentiated from transformed progenitor cells. Our previous research demonstrates that SLCCs are inducible by increasing Genomic instability in cancer cells. In this study, to block the emergence of SLCCs, aminoethyl isothiourea （AET）, a compound that clears free radicals and is used to protect patients from radioactive exposure, was used as an agent that maintains genomic stability in combination with mitomycin C （MMC）, a commonly used chemotherapeutic drug that damages DNA. Using a rabbit tumor model with VX2 hepatic carcinoma, we found that MMC alone increased lung metastases and disadvantaged survival outcome, but the combination of MMC and AET reversed this effect and even prolonged overall survival. Moreover, in a VX2 xenograft model by immunocompromised mice, MMC alone enriched tumor-initiating cells, but the administration of MMC in combination with AET eliminated tumor cells effectively. Furthermore, MMC alone enhanced Genomic instability, but MMC combined with AET attenuated the extent of Genomic instability in primary VX2 tumor tissue. Taken together, our data suggest that the genomic protector AET can inhibit the induction of SLCCs, and this combination treatment by AET and cytotoxic agents should be considered as a promising strategy for future clinical evaluation.

关键词： rabbit VX2 liver tumor mitomycin C AET stem-like cancer cells Genomic instability

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Generation and repair of AID-initiated DNA lesions in B lymphocytes

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Frontiers of Medicine 2014年第2期8卷 201-216页

作者： Zhangguo Chen Jing H. Wang Integrated Department of Immunology University of Colorado Anschutz Medical Campus and National Jewish Health Denver CO 80206USA

Activation-induced deaminase （AID） initiates the secondary antibody diversification process in B lymphocytes. In mammalian B cells, this process includes somatic hypermutation （SHM） and class switch recombination （CSR）, both of which require AID. AID induces U：G mismatch lesions in DNA that are subsequently converted into point mutations or DNA double stranded breaks during SHM/CSR. In a physiological context, AID targets immunogiobulin （Ig） loci to mediate SHM/CSR. However, recent studies reveal genome-wide access of AID to numerous non-Ig loci. Thus, AID poses a threat to the genome of B cells if AID-initiated DNA lesions cannot be properly repaired. In this review, we focus on the molecular mechanisms that regulate the specificity of AID targeting and the repair pathways responsible for processing AID-initiated DNA lesions.

关键词： class switch recombination somatic hypermutation activation-induced deaminase DNA repair Genomic instability

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