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. Author manuscript; available in PMC: 2018 Jul 11.
Published in final edited form as: Semin Oncol. 2017 Jul 11;44(2):101–112. doi: 10.1053/j.seminoncol.2017.06.005

Table 14.

Role of soluble factors secreted by stromal cells in mediating chemoresistance

Cell type/soluble factor Consequence Reference/s
Galectin-3, galactose-binding lectin Galectin-3 implicated in the development of chemoresistance in several solid as well as hematological cancers (59)
B-ALL/Galectin-3 Galectin-3 protects ALL cells by auto-induction of galectin-3 mRNA and activation of the NFκB pathway and Wnt/β-catenin signaling pathway (178,179)
Ph+ B-ALL/Galectin-3 Galectin-3 transcript levels upregulated in Ph+ B-ALL cells that had developed resistance to tyrosine kinase inhibitor nilotinib (180)
CML/Galectin-3 Galectin-3 induced multi-drug resistance by activation of Akt and ERK and preventing apoptosis (181)
Multiple myeloma/Galectin-3 Galectin-3 implicated in chemoresistance mechanisms
Chemoprotective factor/ALL This soluble factor induces an increase in calcium influx into mitochondria, which leads to an increase in reactive oxidation species (ROS) in ALL cells. Cells respond by undergoing a redox adaptation to decrease ROS, thereby reducing ALL sensitivity to drug treatment (77)
Chemoprotective factor/AML This soluble factor promotes chemoresistance by blocking the activity of equilibrative nucleoside transporter (ET1) which regulates cytarabine incorporation inside the cell (182)