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Aurora A Kinase Plays a Key Role in Mitosis Skip during senescence Induced by Ionizing Radiation

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Biomedical and Environmental Sciences 2023年第10期36卷 903-916页

作者： ZHANG Xu Rui ZHANG Tong Shan ZHANG Ya Nan HUA Jun Rui WANG Ju Fang HE Jin Peng Key Laboratory of Space Radiobiology of Gansu Province&CAS Key Laboratory of Heavy Ion Radiation Biology and Medicine Institute of Modern PhysicsChinese Academy of SciencesLanzhou 730000GansuChina National-Local Joint Engineering Research Center of Biodiagnostic&Biotherapy The Second Affiliated HospitalXi’an Jiaotong UniversityXi’an 710004ShaanxiChina University of Chinese Academy of Sciences Beijing 100049China

Objective To investigate the fate and underlying mechanisms of G2 phase arrest in cancer cells elicited by ionizing radiation(IR).Methods Human melanoma A375 and 92-1 cells were treated with X-rays radiation or Aurora A inhibitor MLN8237(MLN)and/or p21 depletion by small interfering RNA(si RNA).Cell cycle distribution was determined using flow cytometry and a fluorescent ubiquitin-based cell cycle indicator(FUCCI)system combined with histone H3 phosphorylation at Ser10(p S10 H3)detection.senescence was assessed using senescence-associated-β-galactosidase(SA-β-Gal),Ki67,andγH2AX staining.Protein expression levels were determined using western blotting.Results Tumor cells suffered severe DNA damage and underwent G2 arrest after IR treatment.The damaged cells did not successfully enter M phase nor were they stably blocked at G2 phase but underwent mitotic skipping and entered G1 phase as tetraploid cells,ultimately leading to senescence in G1.During this process,the p53/p21 pathway is hyperactivated.Accompanying p21 accumulation,Aurora A kinase levels declined sharply.MLN treatment confirmed that Aurora A kinase activity is essential for mitosis skipping and senescence induction.Conclusion Persistent p21 activation during IR-induced G2 phase blockade drives Aurora A kinase degradation,leading to senescence via mitotic skipping.

关键词： Ionizing radiation senescence G2 arrest Tetraploid Mitosis skipping

9-Hydroxy-6,7-dimethoxydalbergiquinol suppresses hydrogen peroxide-induced senescence in human dermal fibroblasts through induction of sirtuin-1 expression

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Asian Pacific Journal of Tropical Biomedicine 2021年第2期11卷 89-96页

作者： Seok-Hee Lim Bing Si Li Ri Zhe Zhu Byung-Min Choi Department of Biochemistry School of MedicineInstitute of BiotechnologyWonkwang University460 Iksandae-roIksanJeonbuk 54538Republic of Korea

Objective:To investigate the potential anti-aging mechanism of9-hydroxy-6,7-dimethoxydalbergiquinol(HDDQ)on hydrogen peroxide(H2O2)-induced oxidative stress in human dermal fibroblasts(HDFs).Methods:The effect of HDDQ on cell viability was assessed by MTT assay,and the effects of HDDQ on senescence-like phenotypes were determined by senescence-associatedβ-galactosidase(SA-β-gal)staining,Western blotting analysis,and a cell proliferation assay.The expression level and activity of sirtuin-1(SIRT1)induced by HDDQ were also measured.Results:HDDQ reversed senescence-like phenotypes in the oxidant-challenged model,through reducing SA-β-gal activity and promoting cell growth.Meanwhile,decreases in ac-p53,p21Cip1/WAF1,and p16Ink4a and an increase in p Rb were observed.HDDQ induced the expression of SIRT1 in a concentration-and time-dependent manner.Moreover,HDDQ inhibited H2O2-induced phosphorylation of Akt by SIRT1 up-regulation and reduced SA-β-gal staining.Conclusions:HDDQ inhibits H2O2-induced premature senescence and upregulation of SIRT1 expression plays a vital role in the inhibition of the senescence phenotype in HDFs.

关键词： 9-Hydroxy-6,7-dimethoxydalbergiquinol Hydrogen peroxide senescence Sirtuin-1 Human dermal fibroblasts

Roles of eIF5A in the immunosurveillance of cellular senescence

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Cancer Biology & Medicine 2022年第11期19卷 1523-1527页

作者： Xiangli Jiang Fabricio Loayza-Puch Department of Thoracic Oncology Tianjin Medical University Cancer Institute&HospitalNational Clinical Research Center for CancerKey Laboratory of Cancer Prevention and TherapyTianjinTianjin's Clinical Research Center for CancerTianjin 300060China Translational Control and Metabolism German Cancer Research Center(DKFZ)Heidelberg 69120Germany

senescence is a cellular stress response program that prevents the proliferation of oncogenically activated, genetically unstable, and/or damaged cells. senescence was first described in 1961, when normal cultured human fibroblasts were found to enter irreversible growth arrest after multiple cell divisions, in a process known as replicative senescence1. Several types of senescence have since been identified, such as stress-induced senescence, oncogene-induced senescence, and virus-induced senescence. Despite having distinct features due to their different triggers, senescent cells share several key features.

关键词： unstable SASP senescence

Role of senescence induction in cancer treatment

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World Journal of Clinical Oncology 2018年第8期9卷 180-187页

作者： Shenghui Qin Bradley A Schulte Gavin Y Wang Department of Pathology and Laboratory Medicine Medical University of South Carolina Developmental Cancer Therapeutics Program of Hollings Cancer Center

Cellular senescence is a form of permanent cell cycle arrest that can be triggered by a variety of cell-intrinsic and extrinsic stimuli, including telomere shortening,DNA damage, oxidative stress, and exposure to chemotherapeutic agents and ionizing radiation. Although the induction of apoptotic cell death is a desirable outcome in cancer therapy, mutations and/or deficiencies in the apoptotic signaling pathways have been frequently identified in many human cancer types,suggesting the importance of alternative apoptosis-independent therapeutic approaches for cancer treatment. A growing body of evidence has documented that senescence induction in tumor cells is a frequent response to many anticancer modalities including cyclin-dependent kinases 4/6 small molecule inhibitor-based targeted therapeutics and T helper-1 cytokine-mediated immunotherapy. This review discusses the recent advances and clinical relevance of therapy-induced senescence in cancer treatment.

关键词： Cellular senescence Cancer treatment Chemotherapy Ionizing radiation Cyclin-dependent kinases 4/6 inhibitor Aurora kinase inhibitor Immunotherapy T helper-1 cells T helper-1 cytokines

Silencing of peroxiredoxin 2 suppresses proliferation and Wnt/β-catenin pathway,and induces senescence in hepatocellular carcinoma

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Oncology Research 2024年第1期32卷 213-226页

作者： XUEGANG YANG XIANHONG XIANG GUOHUI XU SHI ZHOU TIANZHI AN ZHI HUANG Department of Interventional Radiology Sichuan Cancer Hospital and InstituteSichuan Cancer CenterSchool of MedicineUniversity of Electronic Science and Technology of ChinaRadiation Oncology Key Laboratory of Sichuan ProvinceChengdu610041China Department of Interventional Radiology The First Affiliated Hospital of Sun Yat-sen UniversityGuangzhou510080China Department of Interventional Radiology Affiliated Hospital of Guizhou Medical UniversityGuiyang550004China School of Basic Medical Science Guizhou Medical UniversityGuiyang550002China

Hepatocellular carcinoma(HCC),a common malignancy worldwide,still lacks effective clinical treatment.The study aimed to investigate the oncogenes that affect the progression of HCC and their possible mechanisms.In our study,we initially confirmed a higher level of PRDX2 in the bile of HCC patients compared to those with choledocholithiasis by 2-DE,LC-MS,and ELISA.Subsequently,we demonstrated the high expression of peroxiredoxin 2(PRDX2)in HCC based on the TCGA database and clinical sample analysis.Furthermore,PRDX2 overexpression enhanced the viability of HCC cells.And PRDX2 silencing induced senescence of HCC cells.In vivo,knockdown of PRDX2 significantly reduced the weight of xenograft tumors.PRDX2 also was found to activate the Wnt/β-catenin pathway by inducingβ-catenin nuclear translocation.Consequently,we proved that silencing PRDX2 could inhibit proliferation and Wnt/β-catenin pathway while promoting senescence in HCC cells.

关键词： Peroxiredoxin 2 Hepatocellular carcinoma Wnt/β-catenin pathway senescence Proliferation

TaSCL14,a Novel Wheat(Triticum aestivum L.)GRAS Gene,Regulates Plant Growth,Photosynthesis,Tolerance to Photooxidative Stress,and senescence

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Journal of Genetics and Genomics 2015年第1期42卷 21-32页

作者： Kunmei Chen Hongwei Li Yaofeng Chen Qi Zheng Bin Li Zhensheng Li College of Agronomy Northwest A&F University State Key Laboratory of Plant Cell and Chromosome Engineering Institute of Genetics and Developmental BiologyChinese Academy of Sciences

Rates of photosynthesis, tolerance to photooxidative stress, and senescence are all important physiological factors that affect plant development and thus agricultural productivity. GRAS proteins play essential roles in plant growth and development as well as in plant responses to biotic and abiotic stresses. So far few GRAS genes in wheat （Triticum aestivum L.） have been characterized. A previous transcriptome analysis indicated that the expression of a GRAS gene （TaSCL14） was induced by high-light stress in Xiaoyan 54 （XY54）, a common wheat cultivar with strong tolerance to high-light stress. In this study, TaSCL14 gene was isolated from XY54 and mapped on chromosome 4A. TaSCL14 was expressed in various wheat organs, with high levels in stems and roots. Our results confirmed that TaSCL14 expression was indeed responsive to high-light stress. Barley stripe mosaic virus （BSMV）-based virus-induced gene silencing （VIGS） of TaSCL14 in wheat was performed to help characterize its potential functions. Silencing of TaSCL14 resulted in inhibited plant growth, decreased photosynthetic capacity, and reduced tolerance to photooxidative stress. In addition, silencing of TaSCL14 in wheat promoted leaf senescence induced by darkness. These results suggest that TaSCL14 may act as a multifunctional regulator involved in plant growth, photosynthesis, tolerance to photooxidative stress, and senescence.

关键词： Triticum aestivum L. TaSCL14 Photosynthesis Photooxidative resistance senescence BSMV--VIGS

NAC Transcription Factor ORE1 and senescence- Induced BIFUNCTIONAL NUCLEASE1 （BFN1） Constitute a Regulatory Cascade in Arabidopsis

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Molecular Plant 2013年第5期6卷 1438-1452页

作者： Lilian R Matallana-Ramirez Mamoona Rauf Sarit Farage-Barhom Hakan Dortay Gang-Ping Xue Wolfgang Droge-Laser Amnon Lers Salma Balazadeh Bernd Mueller-Roeber University of Potsdam Institute of Biochemistry and Biology KarI-Liebknecht-Straβe 24-25 14476 Potsdam-Golm Germany Department of Postharvest Science of Fresh Produce. Volcani Center Agricultural Research Organization Israel CSIRO Plant Industry Brisbane Australia University of Wurzburg Julius-von-Sachs Institute Julius-von-Sachs Platz 2 97082 Wurzburg Germany Max-Planck Institute of Molecular Plant Physiology 14476 Potsdam-Golm Germany

senescence is a highly regulated process that involves the action of a large number of transcription factors. The NAC transcription factor ORE1 （ANAC092） has recently been shown to play a critical role in positively controlling senescence in Arabidopsis thaliana; however, no direct target gene through which it exerts its molecular function has been identified previously. Here, we report that BIFUNCTIONAL NUCLEASE1 （BFN1）, a well-known senescence-enhanced gene, is directly regulated by ORE1. We detected elevated expression of BFN1 already 2 h after induction of ORE1 in estradiol-inducible ORE1 overexpression lines and 6 h after transfection of Arabidopsis mesophyll cell protoplasts with a 35S：ORE1 construct, ORE1 and BFN1 expression patterns largely overlap, as shown by promoter-reporter gene （GUS） fusions, while BFN1 expression in senescent leaves and the abscission zones of maturing flower organs was virtually absent in ore1 mutant background. In vitro binding site assays revealed a bipartite ORE1 binding site, similar to that of ORS1, a paralog of ORE1. A bipartite ORE1 binding site was identified in the BFN1 promoter; mutating the cis-element within the context of the full-length BFN1 promoter drastically reduced OREl-mediated transactivation capacity in tran- siently transfected Arabidopsis mesophyll cell protoplasts. Furthermore, chromatin immunoprecipitation （CHIP） demon- strates in vivo binding of ORE1 to the BFN1 promoter. We also demonstrate binding of ORE1 in vivo to the promoters of two other senescence-associated genes, namely SAG29/SWEET15 and SINA1, supporting the central role of ORE1 during senescence.

关键词： Arabidopsis thaliana senescence transcription factor ORE1 BFN1 promoter.

Reactive oxygen species and senescence modulatory effects of rice bran extract on 4T1 and NIH-3T3 cells co-treatment with doxorubicin

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Asian Pacific Journal of Tropical Biomedicine 2021年第4期11卷 174-182页

作者： Ummi Maryam Zulfin Ave Rahman Mila Hanifa Rohmad Yudi Utomo Sari Haryanti Edy Meiyanto Cancer Chemoprevention Research Center Faculty of PharmacyUniversitas Gadjah Mada(UGM)Sekip UtaraYogyakarta 55281Indonesia Laboratory of Medicinal Chemistry Department of Pharmaceutical ChemistryFaculty of PharmacyUGMSekip UtaraYogyakarta 55281Indonesia Medicinal Plant and Traditional Medicinal Research and Development Centre Ministry of HealthRepublic of Indonesia Laboratory of Macromolecular Engineering Department of Pharmaceutical ChemistryFaculty of PharmacyUGMSekip UtaraYogyakarta 55281Indonesia

Objective:To determine the effect of rice bran extract(RBE)in combination with doxorubicin on 4 T1 triple-negative breast cancer cells and NIH-3 T3 cells.Methods:RBE was obtained by maceration with n-hexane.The phytochemical profile of RBE was observed using highperformance liquid chromatography.Cytotoxic effect of RBE was evaluated through MTT assay.In addition,flow cytometry was used for cell cycle and apoptosis analysis.Cellular senescence was observed using SA-β-Gal assay and intracellular reactive oxygen species(ROS)levels were evaluated using DCFDA staining.The pro-oxidant property of RBE was also evaluated through 1-chloro-2,4-dinitrobenzene spectrophotometry and molecular docking.Results:RBE was obtained with a yield of 18.42%w/w and contained tocotrienols as the major compound.RBE exerted no cytotoxic effect on 4 T1 and NIH-3 T3 cells.However,RBE in combination with doxorubicin decreased 4 T1 cell viability synergistically(combination indexsenescence on 4 T1 cells.RBE significantly decreased senescence in doxorubicin-treated NIH-3 T3 cells.Additionally,RBE did not increase ROS levels in doxorubicin-treated 4 T1 cells.Meanwhile,the combination of RBE and doxorubicin reduced ROS levels in NIH-3 T3 cells.RBE significantly reduced glutathione-S-transferase activity and alpha-tocotrienol interacted with glutathione-Stransferase in the glutathione binding site.Conclusions:Rice bran may be used as a co-chemotherapeutic agent to improve the therapeutic effectiveness of doxorubicin while protecting against the cellular senescence effects of doxorubicin on healthy cells.

关键词： Rice bran extract ROS senescence Doxorubicin 4T1 NIH-3T3

Correlation of Twist upregulation and senescence bypass during the progression and metastasis of cervical cancer

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Frontiers of Medicine 2014年第1期8卷 106-112页

作者： Tian Wang Yan Li Abidan Tuerhanjiang Wenwen Wang Zhangying Wu Ming Yuan Shixuan Wang Department of Obstetrics and Gynecology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan430030 China

Cervical carcinoma is associated with high propensity for local invasion and lymph node metastasis. However, the molecular alterations that drive progression and metastasis of cervical cancer remain unclear. Cellular senescence has been proposed as the mechanism that protects an organism against cancer progression and metastasis. In addition, Twist, a basic helix-loop-helix transcription factor, has been suggested as an oncogene because it is overexpressed in many types of human cancer. This gene also exhibits a positive function in regulating invasion and metastasis. In this study, Twist was strongly and positively expressed in normal tissue, squamous cell carcinoma （SCC） IA-IIA, and SCC IIB-IIIB （4.3%, 44%, and 88.9%, respectively）. The strong positive expressions of the senescence marker CBX3 were 39.1%, 32%, and 15.6%, respectively. The strong positive expressions of Twist in the SCC groups with or without lymph node metastasis were 80.8% and 50%. For CBX3, such expressions were 7.7% and 29.5%, respectively. Results also showed that the expression of Twist was inversely correlated with that of CBX3. Moreover, the knockdown of Twist with target siRNA in SiHa triggered the induction of the chromatin marker of the cellular senescence CBX3 and senescence-associated p-galactosidase activity. Our results suggested that the expression of Twist increased during the progression and metastasis of cervical cancer. Furthermore, Twist-induced senescence bypass is important in this process.

关键词： cervical cancer senescence Twist CBX3 lymph node metastasis