J Cancer 2018; 9(14):2436-2442. doi:10.7150/jca.24796
LncRNA MALAT1 negatively regulates MDSCs in patients with lung cancer
1. Department of Laboratory Medicine, The Affiliated People's Hospital, Jiangsu University, Zhenjiang, China
2. Department of Immunology, Jiangsu Key Laboratory of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, China
*Current address: Department of Laboratory Medicine, Zhangjiagang Hospital Affiliated to Nanjing University of Chinese Medicine, Zhangjiagang, China
Myeloid-derived suppressor cells (MDSCs) have strong immunosuppressive functions and contribute to the formation of the tumor microenvironment. Long non-coding (Lnc) RNAs are highly important factors associated with tumors and may be used as markers for tumor diagnosis, which is valuable for targeted therapy. LncRNA MALAT1 is expressed in various tissues and plays a critical role in cell proliferation, including tumorigenesis and metastasis. However, the role of MALAT1 in MDSCs is unclear. In this study, we observed an increased proportion of MDSCs and elevated levels of the related molecule arginase-1 (ARG-1) in peripheral blood mononuclear cells (PBMCs) obtained from lung cancer patients. The proportion of CD8+ cytotoxic T lymphocyte (CTL) was significantly decreased in PBMCs from lung cancer patients. Moreover, the proportion of CTL cells was negatively correlated with the proportion of MDSCs. Furthermore, MALAT1 levels were decreased in PBMCs from lung cancer patients. The relative expression of MALAT1 was moderate negatively correlated with the proportion of MDSCs. In vitro results indicate that the knockdown of MALAT1 significantly increased the proportion of MDSCs. Our data provide the first evidence that lncRNA MALAT1 negatively regulates MDSCs and is decreased in PBMCs from lung cancer patients.
Keywords: MDSCs, long non-coding RNA, MALAT1, lung cancer
Zhou Q, Tang X, Tian X, Tian J, Zhang Y, Ma J, Xu H, Wang S. LncRNA MALAT1 negatively regulates MDSCs in patients with lung cancer. J Cancer 2018; 9(14):2436-2442. doi:10.7150/jca.24796. Available from http://www.jcancer.org/v09p2436.htm