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Cancer Cell death Cell cycle Cytoskeleton Exo/endocytosis Differentiation Division Organelles Signalling Stem cells Trafficking
Cell Biology International (2012) 36, 653–659 (Printed in Great Britain)
Anti-miR-155 oligonucleotide enhances chemosensitivity of U251 cell to taxol by inducing apoptosis
Wei Meng*, Ling Jiang†, Lin Lu‡, Haiyan Hu§, Hailang Yu*, Dapeng Ding*, Kun Xiao¶, Wenling Zheng*, Hongbo Guo‖1 and Wenli Ma*1
*Institute of Genetic Engineering, Southern Medical University, Guangzhou, Peoples Republic of China, †Department of Hematology, Nanfang Hospital, Southern Medical University, Guangzhou, Peoples Republic of China, ‡Department of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou, Peoples Republic of China, §Department of Hematology, Zhujiang Hospital, Southern Medical University, Guangzhou, Peoples Republic of China, ¶Department of Epidemiology, Mailman School of Public Health, Columbia University Medical Center, New York, NY 10032, U.S.A., and ‖Department of Neurosurgery, Institute of Neuroscience, Key Laboratory of Guangdong province, Zhujiang Hospital Southern Medical University, Guangzhou, Peoples Republic of China


The oncogene, microRNA-155, is significantly elevated in GBM (glioblastoma multiforme), regulating multiple genes associated with cancer cell proliferation, apoptosis and invasiveness. Thus, miR-155 can theoretically become a target for enhancement of the chemotherapy in cancer. Down-regulating miR-155 to enhance the effect of taxol has not been studied in human GBM. Human GBM U251 cells were treated with taxol and the miR-155 inhibitor alone or in combination. IC50 values were dramatically decreased in cells treated with miR-155 inhibitor combined with taxol, to a greater extent than those treated with taxol alone. Furthermore, the miR-155 inhibitor significantly enhanced apoptosis in U251 cells. The data suggest that miR-155 blockage increased the chemosensitivity to taxol in GBM cells, making combined treatment an effective therapeutic strategy for controlling the growth by inhibiting EAG1 expression.


Key words: apoptosis, glioblastoma multiforme (GBM), miR-155, taxol, U251 cell

Abbreviations: DMEM, Dulbecco's modified Eagle's medium, FBS, foetal bovine serum, GBM, glioblastoma multiformes, miRNAs, microRNAs, MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide, RT, reverse-transcriptase

1To whom correspondence should be addressed (email Mengwei_126@126.com).


Received 28 December 2010/11 September 2011; accepted 26 January 2012

Published as Cell Biology International Immediate Publication 26 January 2012, doi:10.1042/CBI20100918


© The Author(s) Journal compilation © 2012 International Federation for Cell Biology


ISSN Print: 1065-6995
ISSN Electronic: 1095-8355
Published by Portland Press Limited on behalf of the International Federation for Cell Biology (IFCB)