MiR- 150 deletion promotes lung tumor growth by upregulating P-STAT3 and ROS in MDSCs

Lung cancer is the second most common cancer in the world. Myeloid-derived suppressor cells (MDSCs) are important cell populations in the microenvironment of lung cancer, which affects the development and treatment of lung cancer. A large number of studies have shown that miRNA can regulate MDSCs, promoting tumor development. Here we aim to explore the role of miR- 150 on MDSCs in lung tumors. We established lung tumor models by injecting miR- 150 knock-out (miR- 150 KO) mice with LLC subcutaneously. MiR- 150 deletion promoted tumor growth and increased the ratio of MDSCs in tumors. In addition, knockdown of miR- 150 resulted in high serum levels of IL- 6 and G-CSF and promoted the expression of suppressive-associated molecules in MDSCs. In vitro, inhibition of miR- 150 led to increased expression of ROS, IRE1α and P-STAT3 in MDSCs. In vivo administration of STAT3 inhibitor significantly inhibited tumor growth in miR- 150 KO mice and reduced ROS level in tumor MDSCs. Our results indicated that miR- 150 deletion promotes lung tumor growth by upregulating P-STAT3 and ROS in MDSCs, suggesting that STAT3 inhibitors are effective in blocking the production of ROS in MDSCs lacking miR- 150.