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Home > Archive>Volume , Issue 5, 2012 >62-68. DOI:10.3969/j.issn.1005-4847.2012.05.014
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Esophageal cancer EC109 cells induce mast cell migration in a mouse model
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    Abstract:

    Objective To establish an experimental mouse model of mast cell (MC) migration, and explore the killing mechanism of chemotherapeutic drug As2O3 on human esophageal carcinoma EC109 cell line. MethodsMouse mast cell (MC) subsets were defined on the basis of neutral protease composition and immunofluorescence staining, and the distribution image of DNA content in esophageal carcinoma cells was analyzed by propidium iodide labeling and flow cytometry. Secretory granules in MC were observed by laser scanning confocal microscopy. The MC migration from the gut to peritoneal cavity after induction treatments were observed by immunohistochemistry. Results① According to the distribution of flow cytometric dot plot analysis, the mouse MCs were divided into three immunophenotypes:tryptase-positive and chymase-negative MCs (MC T); chymase-positive and tryptase-negative MCs (MC C), and both tryptase-positive and chymase-positive MCs (MC TC). The amount of MC T cells is apparently more than that of MC TC and MC C cells (P<0.05). The laser scanning confocal microscopic observation revealed that all the three subtypes of MCs contained profuse secretory granules distributed in the inner membrane just ready for budding into the extracellular space. ② The mouse MCs migrated from the intestinal tissue into the peritoneal cavity after the induction treatment. The trypsin-induced MC migration was more intensive than that induced by esophageal cancer cells and As2O3. ③ The MC migration into peritoneal cavity may be related to cancer cell cycle transition from S phase to G2/M phase. As2O3 could delay esophageal cancer cell cycle in G0/G1 phase and impeded cells cycle into S phase, thus inhibiting the growth of esophageal cancer cells. Conclusions The esophageal cancer cells injected into the peritoneal cavity of mice mainly induce T MCs to be involved into immune responses. At the presence of MCs in vivo, the effect of As2O3 on tumor cell growth is mainly to delay the cell cycle from G0/G1 phase to S phase, or delay the transition from G2/M phase into cell division.

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