那迪, 郭澎涛, 徐岩, 刘福囝, 王振宁, 邢承忠, 徐惠绵. 胃癌细胞与腹膜间皮相互作进用促腹膜纤维化致腹膜转移的研究[J]. 中国肿瘤临床, 2012, 39(22): 1716-1718. DOI: 10.3969/j.issn.1000-8179.2012.22.008
引用本文: 那迪, 郭澎涛, 徐岩, 刘福囝, 王振宁, 邢承忠, 徐惠绵. 胃癌细胞与腹膜间皮相互作进用促腹膜纤维化致腹膜转移的研究[J]. 中国肿瘤临床, 2012, 39(22): 1716-1718. DOI: 10.3969/j.issn.1000-8179.2012.22.008
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Di NA, Pengtao GUO, Yan XU, Fu-nan LIU, Zhenning WANG, Chengzhong XING, Huimian XU. Interactions between Gastric Cancer Cells and Human Peritoneal Mesothelial Cells Causing Peritoneal Fibrosis and Carcinomatosis[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2012, 39(22): 1716-1718. DOI: 10.3969/j.issn.1000-8179.2012.22.008
Citation: Di NA, Pengtao GUO, Yan XU, Fu-nan LIU, Zhenning WANG, Chengzhong XING, Huimian XU. Interactions between Gastric Cancer Cells and Human Peritoneal Mesothelial Cells Causing Peritoneal Fibrosis and Carcinomatosis[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2012, 39(22): 1716-1718. DOI: 10.3969/j.issn.1000-8179.2012.22.008
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胃癌细胞与腹膜间皮相互作进用促腹膜纤维化致腹膜转移的研究

Interactions between Gastric Cancer Cells and Human Peritoneal Mesothelial Cells Causing Peritoneal Fibrosis and Carcinomatosis

    摘要
  • 摘要:
      目的   研究间皮细胞对胃癌细胞的抵御作用, 模拟游离癌细胞在接触腹膜前通过其分泌物导致的腹膜增厚、纤维化的过程, 同时观察了间皮细胞对胃癌细胞迁移及侵袭能力的反作用。
      方法  用荧光显微镜观察共培养时间皮细胞对胃癌细胞的抵御作用; 体内实验观察腹膜变化; 电镜、光镜下观察体外实验中间皮层在胃癌-腹膜相互作用中的损伤和细胞骨架变化; 采用Millicell小室共培养观察间皮细胞对胃癌细胞迁移及侵袭能力的反作用。
      结果  正常间皮细胞可防止肿瘤细胞对于腹膜的粘附, 受损脱落后胃癌细胞可轻易粘附。体内外实验均显示接触胃癌细胞上清后腹膜间皮细胞受损、凋亡, 并且受损残余的间皮可以反作用于癌细胞, 使其迁移转移力提高。
      结论  正常间皮细胞可以抵御胃癌细胞的侵袭, 受损伤刺激后的间皮细胞可以反作用于胃癌细胞促进其迁移及侵袭。

     

    Abstract:
      Objective   This study aims to describe the mechanism by which gastric cancer cells lead to an early peritoneal metastasis.
      Methods   Injured mesothelial cells were examined by fluorescence microscopy. A rat's parietal thickness was measured using hematoxylin and eosin staining. Morphological changes in the human peritoneal mesothelial cells (HPMC) were observed under a scanning electron microscope and phase-contrast microscope. The cell migration capacity and the gastric cancer cell infestation were examined using Millicell inserts in a chamber co-culture.
      Results   Mesothelial cells could prevent cancer cell infiltration into the sub-mesothelial connective tissues. Conspicuous morphological changes were observed in the HPMC after the treatment with the gastric cancer cell supernatants. The supernatants induced the cytoskeleton reconstruction of HPMC. The injured mesothelial cells promoted invasion and metastasis in the gastric cancer cells.
      Conclusion   These findings indicate that gastric cancer cells can induce peritoneal fibrosis through supernatants during early peritoneal metastasis. However, the injured mesothelial cells can upregulate invasion and metastasis in gastric cancer cells.

     

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