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| 1 | Autophagy inhibition by chloroquine sensitizes HT-29 colorectal cancer cells to concurrent chemoradiation显示文摘AIM:To investigate whether the inhibition of autophagy by chloroquine(CQ)sensitizes rectal tumors to radiation therapy(RT)or concurrent chemoradiation(chemoRT).METHODS:In vitro,HCT-116 and HT-29 colorectal cancer(CRC)cell lines were treated as following:(1)PBS;(2)CQ;(3)5-fluorouracil(5-FU);(4)RT;(5)CQ and RT;(6)5-FU and RT;(7)CQ and 5-FU;and(8)5-FU and CQ and RT.Each group was then exposed to various doses of radiation(0-8 Gy)depending on the experiment.Cell viability and proliferative capacity were measured by3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)and clonogenic assays.Clonogenic survivalcurves were constructed and compared across treatment groups.Autophagy status was determined by assessing the LC3-Ⅱto LC3-Ⅰratio on western blot analysis,autophagosome formation on electron microscopy and identification of a perinuclear punctate pattern with GFPlabeled LC3 on fluorescence microscopy.Cell cycle arrest and cell death were evaluated by FACS and AnnexinⅤanalysis.All experiments were performed in triplicate and statistical analysis was performed by the student’s t test to compare means between treatment groups.RESULTS:RT(2-8 Gy)induced autophagy in HCT-116and HT-29 CRC cell lines at 4 and 6 h post-radiation,respectively,as measured by increasing LC3-Ⅱto LC3-Ⅰratio on western blot.Additionally,electron microscopy demonstrated autophagy induction in HT-29 cells24 h following irradiation at a dose of 8 Gy.Drug treatment with 5-FU(25μmol/L)induced autophagy and the combination of 5-FU and RT demonstrated synergism in autophagy induction.CQ(10μmol/L)alone and in combination with RT effectively inhibited autophagy and sensitized both HCT-116 and HT-29 cells to treatment with radiation(8 Gy;P<0.001 and 0.00001,respectively).Significant decrease in clonogenic survival was seen only in the HT-29 cell line,when CQ was combined with RT at doses of 2 and 8 Gy(P<0.5 and P=0.05,respectively).There were no differences in cell cycle progression or Annexin V staining upon CQ addition to RT.CONCLUSION:Autophagy inhibition by CQ increases CRC cell sensitivity to concurrent treatment with 5-FU and RT in vitro,suggesting that addition of CQ to chemoRT improves CRC treatment response. | Caitlin A Schonewolf Monal Mehta Devora Schiff Hao Wu Bruce G Haffty Vassiliki Karantza Salma K Jabbour | 2014 | World Journal of Gastrointestinal Oncology2014，6，3： | 12 |
| 2 | The biology of chemokines and their receptors显示文摘 | Devora R Zlotnik A | 2000 | Annu Rev Immunol2000，18，： | 1 |
| 3 | The biology of chemokines and their receptors显示文摘 | Devora R Zlotnik A | 2000 | Annu Bey Immunol2000，18，： | 1 |
| 4 | Severe hyperthyroidism: aetiology, clinical fea- tures and treatment outcome 显示文摘 | Iglesias P Devora O | 2010 | Clin Endocrinol ( Oxf )2010，72，4： | 1 |
| 5 | Serological evidence of Mycoplasma pneumoniae infection in acute exacerbation of COPD显示文摘 | David Lieberman Devora Lieberman M. Ben-Yaakov O. Shmarkov Y. Gelfer R. Varshavsky B. Ohana Z. Lazarovich I. Boldur | 2002 | Diagnostic Microbiology & Infectious Disease2002，，1： | 1 |
| 6 | The biology of chemokine and their receptors and chemokine beyond inflamation显示文摘 | Horuk R Zlotnik A Devora R | 1998 | Nature1998，393，： | 1 |
| 7 | The biology of chemokines and their receptors显示文摘 | Devora R Zlotnik A | 2000 | Annu Rev Immunol2000，18，： | 1 |
| 8 | The biology of ehemokines and their receptors显示文摘 | Devora R Zlotnik A | 2000 | Annu Rev Immunol2000，18，： | 1 |
| 9 | Acute gerital postatitis by Ralstonia pickettii:clinical and epidemiohensol consderations of evepcinal observation显示文摘 | Devora RO de Diego GQ Hermando RS | 2009 | Med Clin(Bare)2009，133，7： | 1 |
| 10 | The biology of chemokines andtheir receptors 显示文摘 | Zlotnik A | 2000 | Annu Rev Immunol2000，18，： | 1 |
| 11 | Collaborative pharmacy practice: an idea whose time has come 显示文摘 | Devora Mitrany Renwyck Elder | 1999 | Journal of Managed Care Pharmacy1999，5，6： | 1 |
| 12 | Lungkine, a novel CXC chemokine, specifically expressed by lung bronchoepithelial cells显示文摘 | Devora L Stephen D Yuming Xu | 1999 | J of Immunol1999，162，9： | 1 |
| 13 | The biology of chemokines and their receptors 显示文摘 | Zlotnik A | 2000 | Annu Rev Immunol2000，18，： | 1 |
| 14 | Detachment of the Glycolytic Enzymes, Phosphofructokinase and Aldolase, from Cytoskeleton of Melanoma Cells, Induced by Local Anesthetics显示文摘 | Devora Schwartz Rivka Beitner | 2000 | Molecular Genetics and Metabolism2000，，2： | 1 |
| 15 | Telomere aggregateformation in placenta specimens of pregnancies compli-cated with pre-eclampsia显示文摘 | Rivka SH Moshe F Devora K | 2009 | Cancer Genet Cytogenet2009，195，： | 1 |
| 16 | The biology of chemokines and their recepters显示文摘 | Rossi Devora Zlotnik Alber | 2000 | Annual Reviews Immunology2000，18，1： | 1 |
| 17 | Biosynthesis of eicosapentaenoic acid in the microalgaPorphyridium cruentum. I: The use of externally supplied fatty acids显示文摘 | Devora Shiran Inna Khozin Yair M. Heimer Zvi Cohen | 1996 | Lipids1996，，12： | 1 |
| 18 | Medium-chain acyl-CoA dehydrogenase deficiency: prevalence of ACADM pathogenic variants c.985A>G and c.199T>C in a healthy population in Rio Grande do Sul, Brazil显示文摘Objectives::To investigate the prevalence of ACADM pathogenic variants, c.985A>G and c.199T>C, for medium chain acyl CoA dehydrogenase deficiency (MCADD) in a healthy population in the southern region of Brazil. Methods::This was an observational cross-sectional study with a convenience sampling strategy. The participants were recruited from the blood bank of the Hospital de Clínicas of Porto Alegre, Brazil. A total of 1000 healthy individuals from the state of Rio Grande do Sul were included. Genotyping for the c.199T>C and c.985A>G variants was performed using real-time polymerase chain reaction (PCR) and the PCR-restriction fragment length polymorphism (RFLP) technique, respectively. Individuals considered heterozygous for c.985A>G were subjected to additional acylcarnitine profile analysis using tandem mass spectrometry. Carrier frequency was obtained by calculating the ratio of heterozygous individuals to the total number of individuals analyzed and reported with a 95% confidence interval. Allele and genotype frequencies were calculated based on the Hardy-Weinberg equilibrium.Results::The c.985A>G variant was detected as heterozygotes in three individuals (frequency of the heterozygous genotype = 1:333, allele frequency= 0.0015, minimum frequency of MCADD= 1:444,444) whose acylcarnitine profiles were within normal limits. The c.199T>C variant was not identified.Conclusions::Considering the small sample size and associated allelic heterogeneity with MCADD, these findings are believed to denote the rarity or underdiagnosis of MCADD in southern Brazil. This study provides evidence for the need for further investigation to ascertain the contribution of these diseases to child morbidity and mortality in the country. | Mariana Lopes dos Santos Devora Natalia Randon Fernanda Hendges de Bitencourt Fernanda Sperb-Ludwig Fernanda Sales Luiz Vianna Carmen Regia Vargas Angela Sitta Ida Vanessa Doederlein Schwartz | 2022 | Reproductive and Developmental Medicine2022，6，2： | 0 |
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