Japanese scholars have discovered that sugar chains can increase tumors and hope to develop new anticancer drugs that inhibit tumor growth.
May 16, 2018 Source: Science and Technology Daily
Window._bd_share_config={ "common":{ "bdSnsKey":{ },"bdText":"","bdMini":"2","bdMiniList":false,"bdPic":"","bdStyle":" 0","bdSize":"16"},"share":{ }};with(document)0[(getElementsByTagName('head')[0]||body).appendChild(createElement('script')) .src='http://bdimg.share.baidu.com/static/api/js/share.js?v=89860593.js?cdnversion='+~(-new Date()/36e5)];The reporter recently learned from a joint team of the Japanese Institute of Physical Chemistry and Fukushima Prefectural Medical University that the researchers used mouse studies to find that the sugar chain "α2,6-sialic acid" of the adhesion molecule PECAM on the vascular endothelial cell membrane can regulate tumors. Angiogenesis, which promotes tumor enlargement. The research results have recently been published in the British magazine Oncogene.
The tumor releases vascular endothelial growth factor (VEGF), which forms new blood vessels inside the tumor, thereby obtaining oxygen and nutrients, increasing the number of cells, and further increasing the tumor. Up to now, although an angiogenesis inhibitor targeting vascular endothelial growth factor and its receptor pathway has been developed as an anticancer drug, it is effective only for primary cancer and has no effect on cancer metastasis. One of the reasons why angiogenesis inhibitors are difficult to obtain efficacy is that the metabolism of tumors in a hypoxic microenvironment is reprogrammed to adapt to the new environment of hypoxia and hypoglycemia, so that the tumor continues to increase.
Vascular endothelial cells are cells that form the luminal side of the blood vessel, and the luminal side is covered by proteoglycan and glycoprotein-derived sugar chains. However, in physiology and pathology, how sugar chains of adhesion molecules in vascular endothelial cells play a role in angiogenesis has not been elucidated.
This time, the research team transplanted tumor cells into "α2,6-sialic acid"-deficient mice and wild mice, and observed the size of the tumor and the changes in angiogenesis in the tumor. As a result, it was found that the proliferation of tumors in the deficient mice was significantly decreased as compared with the wild mice. In defective mice, many vascular endothelial cells within the tumor die. After α2,6-sialic acid deficiency, PECAM can not stay on the cell surface, and vascular endothelial cells are more likely to die by transmitting abnormal signals.
This study showed that α2,6-sialic acid is one of the decisive survival factors of tumor blood vessels. Currently, the research team is exploring low molecular compounds that mimic α2,6-sialic acid. If a selective compound that inhibits PECAM interaction is found, it is expected to be a novel angiogenesis inhibitor that inhibits tumor growth. (Reporter Chen Chao)
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