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Effect of 80.55 MeV//u^(12)C^(6+) Ions on Radiosensitivity and cell cycle of Human Hepatoma cell Lines

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Plasma Science and Technology 2008年第2期10卷 245-249页

作者：魏巍李文建郭传玲荆西刚金晓东苏旭 Institute of Modern Physics Chinese Academy of Sciences Lanzhou 730000 China Graduate School of the Chinese Academy of Sciences Beijing 100039 China Institute of Modern Physics Chinese Academy of Sciences Lanzhou 730000 China National Institute for Radiological Protection China CDC Beijing 100088 China

In this paper, the relationship between radiosensitivity, cell cycle alteration and the change of apoptosis in different human hepatoma cell lines irradiated by heavy ions were studied with the aim of building up the base data for clinical therapy. Exponentially growing hepatoma cell lines were irradiated by 80.55 MeV/u12C6＋ ions at a dose of 0 Gy, 0.5 Gy, 1 Gy, 2 Gy, 4 Gy and 8 Gy. The radiosensitivity was assessed by means of the colony-forming assay. The DNA content, the percentage of each cell-cycle phase and the apoptosis rate were obtained with flow cytometry methods. After the irradiation, the SF2 （survival fraction at 2 gray） of SMMC-7721 cells were evidently lower than that of HepG2 cells. The S phase arrest, G2/M phase arrest delay and the apoptosis in the two hepatoma cell lines varied with the increase of the dose and repair time. The heavy ions could obviously kill the human hepatoma cell lines. Compared to HepG2 cells, SMMC-7721 cells were more radiosensitive to 12C^6＋ ions.

关键词： heavy ions human hepatoma cell lines radiosensitivity cell cycle cell apoptosis

Xiaokeping-containing serum suppresses high-glucose-induced proliferation of mesangial cells involved in the regulation of cell cycle progression and the p38 mitogen-activated protein kinase pathway

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Journal of Traditional Chinese Medicine 2021年第1期41卷 44-50页

作者： XIN Chuanwei XIA Zhongni YANG Bo LU Lisong Department of Pharmacy Zhejiang Academy of Traditional Chinese MedicineTongde Hospital of Zhejiang ProvinceHangzhou 310012China

OBJECTIVE: To investigate the efficacy of Xiaokeping(XKP)-containing serum on the proliferation of high-glucose-induced mesangial cells(MCs)and the potential underlying ***: XKP-containing serum was prepared by the intragastric administration of XKP in ***-1 cells were cultured with normal glucose(NC group), high glucose(HG group), and high glucose with different XKP concentrations. cell proliferation was assessed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay,and the cell cycle distribution was detected by flow cytometry. The expression of p38 mitogen-activated protein kinase(p38 MAPK) pathway components in MCs was detected by Western blotting and quantitative real-time polymerase chain ***: The MC proliferation level in the high-glucose group was significantly higher than that in the normal control group, and XKP suppressed the HG-induced proliferation of MCs dose dependently. Moreover, flow cytometry revealed that XKP blocked cell cycle progression by inducing cell cycle arrest in G1 phase and inhibiting S phase entry. XKP down-regulated the protein and m RNA expression of p38 MAPK in MCs(P cell cycle arrest at G1 phase and inhibiting S phase entry. The underlying mechanism involves the down-regulation of the p38 MAPK signaling pathway, providing a theoretical basis for the use of XKP to treat diabetic kidney disease.

关键词： Mesangial cells cell proliferation cell cycle p38 mitogen-activated protein kinase Xiaokeping mixture

Herbal formula Renshenwuweizi decoction induces p53-mediated cell cycle arrest and apoptosis in A549 cells

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Journal of Traditional Chinese Medicine 2020年第5期40卷 766-773页

作者： Yu Shiting Zhang Wanying Yang Junjie Zhao Wenxue Liu Meichen Zhao Daqing Bai Xueyuan Wang Siming Jilin Ginseng Academy Changchun University of Chinese MedicineChangchun 130117China

OBJECTIVE:To investigate the effect of Renshenwuweizi decoction(RSWWZ decoction)on the growth of non-small cell lung cancer cells in ***:A549 non-small cell lung cancer cells were divided into two groups:control and RSWWZ decoction treatment *** Counting Kit-8 was used to measure the inhibitory effect of RSWWZ decoction on the growth of A549 cells.4’,6-diamidino-2-phenylindole staining and Annexin V-fluorescein isothiocyanate/propidium iodide double staining were used to investigate apoptosis in A549 cells following RSWWZ decoction treatment,and the mitochondrial membrane potential of treated cells was detected with Rhodamine *** cycle progression was analyzed by flow *** m RNA levels of p53,Bax,B-cell lymphoma-2(Bcl-2)and p21 were measured by quantitative real-time reverse transcription polymerase chain *** protein expressions of p53,Bax,Bcl-2,p21,cyclin-dependent kinases 2(CDK2),and cyclin A were detected by Western ***:RSWWZ decoction reduced the viability of A549 cells in a dose-dependent manner by inducing apoptosis and decreased mitochondrial membrane *** decoction increased p53 and Bax expression and decreased Bcl-2 expression in a dose-dependent *** decoction also induced an S-phase cell cycle arrest by increasing p21 and decreasing cyclin A and CDK2 ***:In vitro experiments revealed that the Renshenwuweizi decoction-induced decrease in A549 cell proliferation was achieved by inducing apoptosis and S-phase cell cycle arrest via the p53 *** findings provide the experimental basis for Renshenwuweizi decoction treatment of lung cancer.

关键词： Carcinoma,non-small-cell lung A549 cells Apoptosis cell cycle Membrane potential,mitochondrial Signal transduction Renshenwuweizi decoction

Inhibitory Effects of Berberine on the Activation and cell cycle Progression of Human Peripheral Lymphocytes

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cellular & Molecular Immunology 2005年第4期2卷 295-300页

作者： Lihui Xu Yi Liu Xianhui He Key Laboratory of Ministry of Education for Tissue Transplantation and Immunology College of Life Science and Technology Jinan University Guangzhou 510632 China Institute of Bioengineering Jinan University Guangzhou 510632 China Department of Dermatopathology Institute of Dermatology Chinese Academy of Medical Sciences and Peking Union Medical College Nanjing 210042 China

The immunosuppressive property of berberine, an isoquinoline alkaloid, has been well documented, but the mechanism of its action on lymphocytes has not been completely elucidated. The present study is to investigate the effect of berberine on the activation and proliferation of lymphocytes, in particular T lymphocytes. Whole peripheral blood from healthy donors was stimulated with phytohemagglutinin （PHA） alone or phorbol dibutyrate （PDB） plus ionomycin, and the expression of CD69 and CD25 on T lymphocytes was evaluated with flow cytometry. The distribution of cell cycles and cell viability were analyzed by staining with propidium iodide （PI） and 7-aminoactinomycin D （7-AAD）, respectively. The results showed that 100 μmol/L and 50 μmol/L of berberine significantly inhibited CD69 expression on T cells stimulated with PDB plus ionomycin or PHA, whereas the effect of 25 μmol/L berberine was not significant. As the incubation time increased, the extent of inhibition decreased. Similarly, the expression of CD25 was also reduced by berberine in a dose-dependent manner over the concentration range of 25-100 μmol/L. Besides, this alkaloid could block lymphocyte cell cycle progression from G0/G1 phase to S and G2/M phase without phase specificity. Moreover, analysis following 7-AAD staining revealed that berberine had no significant cytotoxicity on lymphocytes. Taken together, berberine significantly inhibits the expression of activation antigens on T lymphocytes and also blocks the progression of cell cycles of lymphocytes, suggesting that berberine may exert immunosuppressive effect through inhibiting the activation and proliferation of T cells.

关键词： berberine lymphocyte activation antigen cell cycle

PADI3 induces cell cycle arrest via the Sirt2/AKT/p21 pathway and acts as a tumor suppressor gene in colon cancer

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Cancer Biology & Medicine 2019年第4期16卷 729-742页

作者： Xiaotian Chang Zhengbin Chai Jiaorui Zou Hongxing Wang Yao Wang Yabing Zheng Hui Wu Chunyan Liu Medical Research Center The First Affiliated Hospital of Shandong First Medical UniversityJinan 250014 Medical Research Center of the Hospital Affiliated to Qingdao University Qingdao 266000China Department of Laboratory Medicine Jinan Infectious Disease HospitalShandong UniversityJinan 250021China

Objective:As a member of the peptidyl arginine deiminase(PAD)family,PADI3 is weakly expressed in colon cancer tissues and highly expressed in adjacent colon cancer ***,the role of PADI3 in colon cancer is *** this study,we investigated the function and molecular mechanism of PADI3 in colon cancer ***:Western blot and real-time PCR were used to detect the expression levels of several ***-8,flow cytometry(FCM)and colony formation assays were used to examine cell proliferation,the cell cycle and colony formation *** analysis was used to study the molecular mechanism of PADI3 in tumorigenesis.A truncation mutation experiment was performed to determine the key functional domain of ***:PADI3 overexpression inhibited cell proliferation and colony formation and led to G1 phase arrest in both HCT116(originating from primary colon cancer)and LoVo(originating from metastatic tumor nodules of colon cancer)***3-expressing HCT116 cells had a lower tumor formation rate and produced smaller tumors than control ***3 significantly decreased Sirtuin2(Sirt2)and Snail expression and AKT phosphorylation and increased p21 expression,and Sirt2 overexpression partly reversed the effects induced by PADI3 *** showed that PADI3 is mainly localized in the *** mutation experiments showed that the C-domain is the key domain involved in the antitumor activity of ***:PADI3 suppresses Snail expression and AKT phosphorylation and promotes p21 expression by downregulating Sirt2 expression in the cytoplasm,and the C-domain is the key domain for its antitumor activity.

关键词： PADI3 Sirt2 colon cancer cell cycle C-domain

Essential functions of iron-requiring proteins n DNA replication, repair and cell cycle contro

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Protein & cell 2014年第10期5卷 750-760页

作者： Caiguo Zhang Department of Biochemistry and Molecular Genetics University of Colorado School of Medicine Aurora CO 80045 USA

Eukaryotic cells contain numerous iron-requiring pro- teins such as iron-sulfur （Fe-S） cluster proteins, hemoproteins and ribonucleotide reductases （RNRs）. These proteins utilize iron as a cofactor and perform key roles in DNA replication, DNA repair, metabolic catalysis, iron regulation and cell cycle progression. Disruption of iron homeostasis always impairs the functions of these iron- requiring proteins and is genetically associated with diseases characterized by DNA repair defects in mam- mals. Organisms have evolved multi-layered mecha- nisms to regulate iron balance to ensure genome stability and cell development. This review briefly pro- vides current perspectives on iron homeostasis in yeast and mammals, and mainly summarizes the most recent understandings on iron-requiring protein functions involved in DNA stability maintenance and cell cycle control.

关键词： iron-requiring protein DNA replication,DNA repair cell cycle iron homeostasis

Regulation of the G1 phase of the mammalian cell cycle

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cell Research 2000年第1期10卷 1-16页

作者： DONJERKOVIC DUBRRAVKA DAVID W SCOTT (Department of Immunology, Holland Laboratory for the Biomedical Sciences, American Red Cross, 15601 Crabbs Branch Way, Rockville, MD) DepartmentofImmunology HollandLaboratoryfortheBiomedicalSciencesAmericanRedCrossRockvilleMDUSA.

In any multi-cellular organism, the balance between cell division and cell death maintains a constant cell number. Both cell division cycle and cell death are highly regulated events. Whether the cell will proceed through the cycle or not, depends upon whether the conditions required at the checkpoints during the cycle are fulfilled. In higher eucaryotic cells, such as mammalian cells, signals that arrest the cycle usually act at a G1 checkpoint. cells that pass this restriction point are committed to complete the cycle. Regulation of the GI phase of the cell cycle is extremely complex and involves many different families of proteins such as retinoblastoma family cyclin dependent kinases, cyclins, and cyclic kinase inhibitors.

关键词： cell cycle cyclin dependent kinase cyclin cyclin kinase inhibitor.

Silencing livin gene by siRNA leads to apoptosis induction,cell cycle arrest,and proliferation inhibition in malignant melanoma LiBr cells

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Acta Pharmacologica Sinica 2007年第12期28卷 1968-1974页

作者： Hao WANG~1,Sheng-shun TAN~(1,4),Xin-yang WANG~2,Dong-hua LIU~1,Chun-shui YU~1,Zhuan-li BAI~1,Da-lin HE~2,Jun ZHAO~3~1 Department of Dermatology,The Second Affliated Hospital of Medical School,Xi'an Jiaotong University,Xi'an 710004,China ~2 Institute ofUrology,Key Laboratory of Environment and Genes Related to Diseases of Ministry of Education,Xi'an Jiaotong University Xi'an 710061,China ~3 Department of Urology,The Medical School Hospital of Qingdao University Qingdao 266003,China Department of Dermatology The Second Affliated Hospital of Medical School Xi'an Jiaotong University Xi'an China Institute of Urology Key Laboratory of Environment and Genes Related to Diseases of Ministry of Education Xi'an Jiaotong University Xi'an China Department of Urology The Medical School Hospital of Qingdao University Qingdao China

Aim:The aim of the present study was to investigate the effects of silencing thelivin gene by small interfering RNA （siRNA） on the expression of livin and theeffects on apoptosis,cell cycle,and proliferation in human malignant melanomaLiBr ***:Three chemically-synthetic siRNA duplexes targeting livinwere transiently transfected into the LiBr cells,and the effects on livin expressionwere detected both at the mRNA level by real-time RT-PCR and at the protein levelby Western *** was evaluated by terminal deoxynucleotidyltransferase-mediated digoxigenin-dUTP nick-end labeling assay,flow cytometricanalysis,and the expression of procaspase-3 and activated caspase-3 analysis byWestern *** cycle was analyzed by flow *** proliferationwas determined by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium ***:One of the 3 designed siRNA could effectively knock down the livinexpression both at the mRNA and protein levels in dose-and time-dependentmanners;100 nmol/L with maximum downregulation on mRNA at 48 h,and on theprotein at 72 h after *** livin could significantly induceapoptosis,arrest cell cycle at the G0/G1phase,and inhibit proliferation in ***,caspase-3 was ***:The livin gene couldserve as a potential molecular target for gene therapy by siRNA for malignantmelanoma.

关键词： livin malignant melanoma siRNA apoptosis cell cycle proliferation

Downregulation of SNRPG induces cell cycle arrest and sensitizes human glioblastoma cells to temozolomide by targeting Myc through a p53-dependent signaling pathway

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Cancer Biology & Medicine 2020年第1期17卷 112-131页

作者： Yulong Lan Jiacheng Lou Jiliang Hu Zhikuan Yu Wen Lyu Bo Zhang Department of Neurosurgery The Second Affiliated Hospital of Dalian Medical UniversityDalian 116023China Department of Neurosurgery Shenzhen People's HospitalSecond Clinical Medical College of Jinan UniversityThe First Affiliated Hospital of Southern University of Science and TechnologyShenzhen 518020China

Objective:Temozolomide(TMZ)is commonly used for glioblastoma multiforme(GBM)***,drug resistance limits its therapeutic effect in GBM ***-binding proteins(RBPs)have vital roles in posttranscriptional *** disturbance of RBP-RNA network activity is potentially associated with cancer development,the precise mechanisms are not fully *** SNRPG gene,encoding small nuclear ribonucleoprotein polypeptide G,was recently found to be related to cancer incidence,but its exact function has yet to be ***:SNRPG knockdown was achieved via short hairpin *** expression profiling and Western blot analyses were used to identify potential glioma cell growth signaling pathways affected by *** tumors were examined to determine the carcinogenic effects of SNRPG on glioma ***:The SNRPG-mediated inhibitory effect on glioma cells might be due to the targeted prevention of Myc and *** addition,the effects of SNRPG loss on p53 levels and cell cycle progression were found to be ***,SNRPG was increased in TMZ-resistant GBM cells,and downregulation of SNRPG potentially sensitized resistant cells to TMZ,suggesting that SNRPG deficiency decreases the chemoresistance of GBM cells to TMZ via the p53 signaling *** data confirmed that SNRPG suppression sensitizes GBM cells to TMZ by targeting Myc via the p53 signaling ***:These results indicated that SNRPG is a probable molecular target of GBM and suggested that suppressing SNRPG in resistant GBM cells might be a substantially beneficial method for overcoming essential drug resistance.

关键词： SNRPG glioblastoma cell cycle temozolomide therapy