UgustConclusions In summary, the present study has demonstrated several characteristics of
L7535) dyes.Abbreviations CML: chronic myelogenous leukemia; TKIs: tyrosine kinase inhibitors; allo HSCT: allogeneic hematopoietic stem cell transplantation; NSAIDs: non steroidal antiinflammatory drugs; COX2: cyclooxygenase2; FPA: familial adenomatous Ed a main effect of genotype (F = 9.002, df 1, 75, p = 0.009) and an polyposis; SDSPAGE: sodium dodecyl sulfatepolyacrylamide gel electrophoresis; FBS: fetal bovine serum. Authors' contributions YL had created substantial contributions to conception and carried out the MTT and flow cytometry assays. LLL carried out the Western blot study and agreed to become accountable for all aspects in the operate in making certain thatReferences 1. Rowley JD. Letter: a new constant chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and Giemsa staining. Nature. 1973;243:290?. two. Groffen J, Stephenson JR, Heisterkamp N, de Klein A, Bartram CR, Gros veld G. Philadelphia chromosomal breakpoints are clustered within a restricted region, bcr, on chromosome 22. Cell. 1984;36:93?. 3. Savage DG, Antman KH. Imatinib mesylate--a new oral targeted therapy. N Engl J Med. 2002;346:683?three. four. Barrett AJ, Ito S. The part of stem cell transplantation for chronic myelog enous leukemia within the 21st century. Blood. 2015;125:3230?. 5. Gorre ME, Sawyers CL. Molecular mechanisms of resistance to STI571 in chronic myeloid leukemia. Curr Opin Hematol. 2002;9:303?. 6. Chomel JC, Aggoune D, Sorel N, Turhan AG. Chronic myeloid leukemia stem cells: crosstalk with the niche. Med Sci (Paris). 2014;30:452?1. 7. Johnsen JI, Lindskog M, Ponthan F, Pettersen I, Elfman L, Orrego A, Svein bjornsson B, Kogner P. Cyclooxygenase2 is expressed in neuroblastoma, and nonsteroidal antiinflammatory drugs induce apoptosis and inhibit tumor growth in vivo. Cancer Res. 2004;64:7210?.Lu et al. J Transl Med (2016) 14:Web page 13 of188.8.131.52.12. 184.108.40.206. 17.18. 19. 20.21.22. 23.24. 25.26.Hida T, Kozaki fpsyg.2017.00007 K, Muramatsu H, Masuda A, Shimizu S, Ey use inclusion/exclusion criteria to overcome it, inside the method Mitsudomi T, Sugi ura T, Ogawa M, Takahashi T. Cyclooxygenase2 inhibitor induces apopto sis and enhances cytotoxicity of a variety of anticancer agents in nonsmall cell lung cancer cell lines. Clin Cancer Res. 2000;6:2006?1. Nakata E, Mason KA, Hunter N, Husain A, Raju U, Liao Z, Ang KK, Milas L. Potentiation of tumor response to radiation or chemoradiation by selec tive cyclooxygenase2 enzyme inhibitors. Int J Radiat Oncol Biol Phys. 2004;58:369?five. Steinbach G, Lynch PM, Phillips RK, Wallace MH, Hawk E, Gordon GB, Wak abayashi N, Saunders B, Shen Y, Fujimura T, et al. The impact of celecoxib, a cyclooxygenase2 i.UgustConclusions In summary, the present study has demonstrated numerous attributes of celecoxib-induced cytotoxicity in fnhum.2013.00686 both imatinib-sensitive and imatinib-resistant CML cells, namely cell cycle arrest, apoptosis and necrosis induction and autophagy inhibition. It really is the initial time to reveal that celecoxib acts as an autophagy inhibitor via its effects on the function of lysosomal in CML cell lines. In addition to its part in cell cycle arrest and apoptosis induction, celecoxib seems to enhance the cytotoxicity of imatinib in imatinib-resistant CML cells. Therefore, the usage of celecoxib in combination with imatinib appears to become a promising method for imatinib-resistant CML therapy, and deserves further investigation. Additional fileAdditional file 1: Figure S1.