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<p>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.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月15日

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  • Anqi Qin,
  • Hao Chen,
  • Fan Xu,
  • Wenting Li,
  • Shuai Guo,
  • Ge Zhang,
  • Aihong Zhang,
  • Aihua Zheng,
  • Feng Tian,
  • Quanhui Zheng

摘要

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.