Mast cells influence soft tissue tumor increase through inflammatory or other proliferative factor in tumor environment.

神经纤维瘤是一种良性肿瘤，主要由雪旺细胞和成纤维细胞组成。肥大细胞散布在肿瘤组织中，提示它们在促进神经纤维瘤的增殖中起着重要作用。我们明确了肥大细胞能显著促进NF1细胞的增殖，并上调TGFb1、SCF和MnSOD的水平。在本研究中，我们观察到了MnSOD与其转录因子核转录因子kappaB的相互作用。我们用免疫印迹的方法明确了NF1细胞与肥大细胞共培养过程中NFkB-P65、磷酸化IKB、磷酸化P65的表达。MnSOD的表达晚于其他蛋白的表达。NF1细胞经脂多糖刺激后MnSOD升高，经曲尼司特(抗过敏药)和BAY11-7082(NFkB抑制剂)刺激后明显下降。因此，这些结果提示，参与细胞间相互作用的可溶性因子可能激活了NFkB信号通路，从而转录了MnSOD。

Neurofibromas are benign tumors that comprise primarily of Schwann cells and fibroblasts. Mast cells have been found scattered in the tumor tissue, and their role in promoting the proliferation of neurofibroma has been suggested. We have clarified that mast cells significantly promoted proliferation of the NF1 cells and upper the levels of TGFb1, SCF and MnSOD. In this study, we observed association between MnSOD and its transcription factor Nuclear factor kappa B. We clarified that NFkB-p65, phospho-IkB, phospho-p65 in co-culture of NF1 cells and mast cells using western blotting. MnSOD was later than the other protein expression. MnSOD in the NF1 cells were increased after LPS stimulation and strongly decreased after tranilast (anti-allergic agent) and BAY11-7082 (NFkB inhibitor) stimulations compared without them. Hence, these results suggest a possibility that soluble factor involved in the cell-cell interaction activates NFkB signaling pathway for transcription of MnSOD.