Ght to constitute a cross-bridge between gal-3 and Wnt signaling. Conclusions: Our results suggest that

Ght to constitute a cross-bridge between gal-3 and Wnt signaling. Conclusions: Our results suggest that gal-3, a key factor mediating BMM-induced drug resistance, could be a novel therapeutic target in acute leukemia. Keywords: Galectin-3, Acute leukemia, Bone marrow mesenchymal stromal cell (BM-MSC), -catenin, Drug resistanceBackground Acute leukemia (AL), mainly consisting of acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL), is currently the major cause of death in hematological malignancies, affecting patients of all ages. Despite ongoing improvements in the outcomes of patients with AL,* Correspondence: [email protected] Equal contributors 1 Bone Marrow Transplantation Center, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China Full list of author information is available at the end of the articleonly 30 -40 of adult ALL patients XAV-939 site achieve long-term, disease-free survival due to drug resistance and disease relapse [1,2]. AML is a heterogeneous disease, and a substantial number of AML patients have quite a low cure rate even after hematopoietic stem cell transplantation [3,4]. Minimal residual disease (MRD), which is widely considered an independent prognostic factor and currently attracts much attention in treatment intervention, has become a vital challenge in the search for a cure for AL [5-7]. In addition, the leukemia niche is believed to play a critical role PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28045099 in the development of MRD.?2015 Hu et al.; licensee BioMed Central. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.Hu et al. Journal of Hematology Oncology (2015) 8:Page 2 ofThe leukemia niche, composed of the osteoblastic and vascular bone marrow niche, provides a home for malignant cells and is responsible for disease relapse as well as treatment resistance. Previous studies have shown that stromal cells in the bone marrow microenvironment (BMM) play an important role in leukemia genesis and progress by secreting various chemicals and contacting signals [8], for example the axis of VCAM-1/VLA-4 [9], SDF-1/CXCR4 [10], and Notch [11], as shown in vitro and in vivo. Since mesenchymal stromal cells (MSCs), an important component of both the solid and hematologic tumor microenvironment [12], give rise to different stromal cell lineages [13]. In our study we used human bone marrow-derived MSCs (hBM-MSCs) to represent a relatively homogeneous BMM stromal cell population with hematopoiesis-supporting capabilities and immuneregulatory properties. Galectin-3 (gal-3), a 30-kDa protein without enzymatic activity, is a member of the -galactoside-specific lectin family. Gal-3 exhibits pleiotropic biological functions especially in tumors. It has roles in cell growth, apoptosis, adhesion, tumor angiogenesis, malignant cell metastasis, cancer-matrix interaction and also cancer drug resistance [14,15]. Recent evidence revealed that gal-3 was up-regulated in Ph+ chronic myeloid leukemia (CML) and in pre-B ALL after conditioning with BM stromal cells [16,17]. Cheng and colleagues [18] reported that in patients with AML, h.