Novel modulation on myeloid-derived suppressor cells (MDSCs) by methionine encephalin (MENK)
Jin Geng1, Ye Yuan2, Xue Jiao3
1Department of Immunology, School of Basic Medical Science, China Medical University, Shenyang 110122, China; Department of Ophthalmology, No. 1 Teaching Hospital, China Medical University, Shenyang 110001, China.
Abstract:
The purpose of this study was to identify the modulatory effect of MENK on MDSCs and to investigate the relationship between this modulation and the expression of opioid receptors. Our results showed that MENK could inhibit the proliferation of MDSCs from both marine bone marrow and spleen. MENK also could promote the expression of opioid receptors MOR and DOR. MENK suppressed the PMN-MDSCs generated from splenocyte while up-regulated M-MDSCs. The stimulation of MENK increased the production of IL-4 secreted by MDSCs from slpenocytes. Our currently data indicated that MENK could suppress the accumulation of MDSCs in tumor-bearing mice via binding to and up-regulating expressions of subunits of opioid receptors. Therefore, it is concluded that MENK, through triggering opioid receptors could exert inhibiting modulation on MDSCs.
Related Concept Videos
Differentiation of Common Myeloid Progenitor Cells
Loss of Tumor Suppressor Gene Functions
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Cancer-Critical Genes II: Tumor Suppressor Genes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Measurement: Derived Units
Higher Derivatives
Derivatives


