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JCI:日发现胃部一种糖链的缺失可致胃癌

  1. 糖链
  2. 胃癌

来源:新华网 2012-11-18 10:52

近日,日本信州大学一个研究小组最新报告说,实验鼠胃黏膜中的一种糖链缺失会引发胃癌,早期胃癌患者胃部这一糖链也出现减少甚至消失,因此可据此寻找预防胃癌的方法。相关论文发表在美国《临床研究杂志》(Journal of Clinical Investigation)网络版上。 糖链是葡萄糖、半乳糖等糖类分子按特定序列形成的链状物。

近日,日本信州大学一个研究小组最新报告说,实验鼠胃黏膜中的一种糖链缺失会引发胃癌,早期胃癌患者胃部这一糖链也出现减少甚至消失,因此可据此寻找预防胃癌的方法。相关论文发表在美国《临床研究杂志》(Journal of Clinical Investigation)网络版上。

糖链是葡萄糖、半乳糖等糖类分子按特定序列形成的链状物。信州大学医学部教授中山淳率领的研究小组研究发现,胃黏膜产生的液体中含有一种糖链,这种糖链含有α型N乙酰氨基葡萄糖。研究人员通过基因技术,培育出胃黏膜不产生这种糖链的小鼠,结果这些小鼠出生5周后,胃和十二指肠接合部的胃黏膜就出现炎症,30周后确认出现癌细胞。研究小组还发现,早期胃癌患者胃部这一糖链也出现减少甚至消失,因此确认这种糖链具有消炎和防止患癌的功能。

中山淳指出,胃癌有90%以上被认为是幽门螺杆菌导致的,他们在2004年曾发现这种糖链能够遏制幽门螺杆菌的增殖。不过此次实验没有让小鼠感染幽门螺杆菌。中山淳说,希望这一发现有助于开发出补充这种糖链的药物从而预防胃癌。(生物谷Bioon.com)

Essential role of gastric gland mucin in preventing gastric cancer in mice

Fumitoshi Karasawa, Akira Shiota, Yukinobu Goso, Motohiro Kobayashi, Yoshiko Sato, Junya Masumoto, Maiko Fujiwara, Shuichi Yokosawa, Takashi Muraki, Shinichi Miyagawa, Masatsugu Ueda, Michiko N. Fukuda, Minoru Fukuda, Kazuhiko Ishihara and Jun Nakayama

Gastric gland mucin secreted from the lower portion of the gastric mucosa contains unique O-linked oligosaccharides (O-glycans) having terminal α1,4-linked N-acetylglucosamine residues (αGlcNAc). Previously, we identified human α1,4-N-acetylglucosaminyltransferase (α4GnT), which is responsible for the O-glycan biosynthesis and characterized αGlcNAc function in suppressing Helicobacter pylori in vitro. In the present study, we engineered A4gnt–/– mice to better understand its role in vivo. A4gnt–/– mice showed complete lack of αGlcNAc expression in gastric gland mucin. Surprisingly, all the mutant mice developed gastric adenocarcinoma through a hyperplasia-dysplasia-carcinoma sequence in the absence of H. pylori infection. Microarray and quantitative RT-PCR analysis revealed upregulation of genes encoding inflammatory chemokine ligands, proinflammatory cytokines, and growth factors, such as Ccl2, Il-11, and Hgf in the gastric mucosa of A4gnt–/– mice. Further supporting an important role for this O-glycan in cancer progression, we also observed significantly reduced αGlcNAc in human gastric adenocarcinoma and adenoma. Our results demonstrate that the absence of αGlcNAc triggers gastric tumorigenesis through inflammation-associated pathways in vivo. Thus, αGlcNAc-terminated gastric mucin plays dual roles in preventing gastric cancer by inhibiting H. pylori infection and also suppressing tumor-promoting inflammation.

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