Oncotarget

Research Papers:

Identification of galectin-1 as a novel mediator for chemoresistance in chronic myeloid leukemia cells

Wu Luo _, Li Song, Xi-Lei Chen, Xiang-Feng Zeng, Jian-Zhang Wu, Cai-Rong Zhu, Tao Huang, Xiang-Peng Tan, Xiao-Mian Lin, Qi Yang, Ji-Zhong Wang, Xiao-Kun Li and Xiao-Ping Wu

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Oncotarget. 2016; 7:26709-26723. https://doi.org/10.18632/oncotarget.8489

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Abstract

Wu Luo1,*, Li Song1,*, Xi-Lei Chen1,*, Xiang-Feng Zeng1, Jian-Zhang Wu2, Cai-Rong Zhu3, Tao Huang1, Xiang-Peng Tan1, Xiao-Mian Lin1, Qi Yang1, Ji-Zhong Wang1, Xiao-Kun Li2, Xiao-Ping Wu1,2

1Institute of Tissue Transplantation and Immunology, Key Laboratory of Functional Protein Research of Guangdong Higher Education Institutes, Key Laboratory of Molecule Immunology and Antibody Engineering of Guangdong Province, Jinan University, Guangzhou, 510632, China

2School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, 325035, China

3Guangzhou Women and Children’s Medical Center, Guangzhou, 510623, China

*These authors have contributed equally to this work

Correspondence to:

Xiao-Ping Wu, e-mail: [email protected]

Keywords: galectin-1, chronic myelogenous leukemia, chemoresistance, MDR1, P38 MAPK

Received: December 03, 2015    Accepted: March 10, 2016    Published: March 30, 2016

ABSTRACT

Multidrug resistance protein-1 (MDR1) has been proven to be associated with the development of chemoresistance to imatinib (Glivec, STI571) which displays high efficacy in treatment of BCR-ABL-positive chronic myelogenous leukemia (CML). However, the possible mechanisms of MDR1 modulation in the process of the resistance development remain to be defined. Herein, galectin-1 was identified as a candidate modulator of MDR1 by proteomic analysis of a model system of leukemia cell lines with a gradual increase of MDR1 expression and drug resistance. Coincidently, alteration of galectin-1 expression triggers the change of MDR1 expression as well as the resistance to the cytotoxic drugs, suggesting that augment of MDR1 expression engages in galectin-1-mediated chemoresistance. Moreover, we provided the first data showing that NF-κB translocation induced by P38 MAPK activation was responsible for the modulation effect of galectin-1 on MDR1 in the chronic myelogenous leukemia cells. Galectin-1 might be considered as a novel target for combined modality therapy for enhancing the efficacy of CML treatment with imatinib.


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