Search

Copyright of Chinese Journal of Oncology is the property of Chinese Journal of Oncology / Zhonghua Zhongliu Zazhi and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Ｏｂｊｅｃｔｉｖｅ 　Ｔｏ ｉｎｖｅｓｔｉｇａｔｅ ｔｈｅ ｆｕｎｃｔｉｏｎ ａｎｄ ｍｅｃｈａｎｉｓｍ ｏｆ ｚｉｎｃ ｆｉｎｇｅｒ ｐｒｏｔｅｉｎ ７５０ （ＺＮＦ７５０） ｉｎ ｅｓｏｐｈａｇｅａｌ ｓｑｕａｍｏｕｓ ｃｅｌｌ ｃａｒｃｉｎｏｍａ （ＥＳＣＣ）． Ｍｅｔｈｏｄｓ　Ｘｅｎｏｇｒａｆｔ ｉｎ ｎｕｄｅ ｍｉｃｅ ｗａｓ ａｐｐｌｉｅｄ ｔｏ ｄｅｔｅｃｔ ｔｈｅ ｔｕｍｏｒｉｇｅｎｅｓｉｓ ｏｆ ＺＮＦ７５０⁃ｄｅｐｌｅｔｅｄ ＥＳＣＣ ｃｅｌｌｓ． Ｗｅｓｔｅｒｎ ｂｌｏｔ ｗａｓ ｐｅｒｆｏｒｍｅｄ ｔｏ ｏｂｓｅｒｖｅ ｔｈｅ ｅｘｐｒｅｓｓｉｏｎ ｏｆ ｄｏｗｎｓｔｒｅａｍ ｔａｒｇｅｔ ｐｒｏｔｅｉｎ ｏｆ ＺＮＦ７５０ ｉｎ ＥＳＣＣ ｃｅｌｌ ｌｉｎｅｓ ａｎｄ ｘｅｎｏｇｒａｆｔ ｔｕｍｏｒ ｔｉｓｓｕｅｓ ｉｎ ｗｈｉｃｈ ＺＮＦ７５０ ｗａｓ ｋｎｏｃｋｅｄ ｄｏｗｎ. ３⁃（４，５⁃ｄｉｍｅｔｈｙｌ⁃２⁃ｔｈｉａｚｏｌｙｌ）⁃２，５⁃ｄｉｐｈｅｎｙｌ⁃２Ｈ ｔｅｔｒａｚｏｌｉｕｍ ｂｒｏｍｉｄｅ （ＭＴＴ） ａｓｓａｙ ｗａｓ ｕｓｅｄ ｔｏ ｄｅｔｅｒｍｉｎｅ ｔｈｅ ｐｒｏｌｉｆｅｒａｔｉｏｎ ｏｆ ＺＮＦ７５０ ｓｔａｂｌｙ ｄｅｐｌｅｔｅｄ ｃｅｌｌｓ ａｆｔｅｒ ｒｅｓｔｏｒａｔｉｏｎ ｏｆ ｉｔｓ ｔａｒｇｅｔ ｐｒｏｔｅｉｎ． Ｒｅｓｕｌｔｓ　Ｔｈｅ ｔｕｍｏｒ ｗｅｉｇｈｔ ｏｆ ｂｌａｎｋ ｃｏｎｔｒｏｌ， ｎｅｇａｔｉｖｅ ｃｏｎｔｒｏｌ ａｎｄ ＺＮＦ７５０ ｋｎｏｃｋｄｏｗｎ ｇｒｏｕｐｓ ｗａｓ １３７±２６ ｍｇ， １６１±３１ ｍｇ ａｎｄ ４６３±８９ ｍｇ， ｒｅｓｐｅｃｔｉｖｅｌｙ， ｗｉｔｈ ａ ｓｔａｔｉｓｔｉｃａｌｌｙ ｓｉｇｎｉｆｉｃａｎｔ ｄｉｆｆｅｒｅｎｃｅ （Ｐ＜０．０１）． Ｔｈｅ ｅｘｐｒｅｓｓｉｏｎｓ ｏｆ Ｋｒｕｐｐｅｌ⁃ｌｉｋｅ ｆａｃｔｏｒ ４ （ＫＬＦ４） ｉｎ ＺＮＦ７５０⁃ｄｅｐｌｅｔｅｄ ＥＳＣＣ ｃｅｌｌｓ ａｎｄ ｉｔｓ ｄｅｒｉｖｅｄ ｔｕｍｏｒ ｔｉｓｓｕｅ ｘｅｎｏｇｒａｆｔ ｉｎ ｎｕｄｅ ｍｉｃｅ ｗｅｒｅ ｓｉｇｎｉｆｉｃａｎｔｌｙ ｄｏｗｎ⁃ｒｅｇｕｌａｔｅｄ． Ｒｅｓｔｏｒａｔｉｏｎ ｏｆ ＫＬＦ４ ｉｎ ＺＮＦ７５０ ｓｔａｂｌｙ ｄｅｐｌｅｔｅｄ ｃｅｌｌｓ ｓｉｇｎｉｆｉｃａｎｔｌｙ ｉｎｈｉｂｉｔｅｄ ｔｈｅ ｃｅｌｌ ｐｒｏｌｉｆｅｒａｔｉｏｎ （Ｐ＜０．０１）． Ｃｏｎｃｌｕｓｉｏｎｓ　ＺＮＦ７５０ ｍａｙ ｂｅ ａ ｎｅｗ ｔｕｍｏｒ ｓｕｐｐｒｅｓｓｏｒ ｉｎ ｔｈｅ ｔｕｍｏｒｉｇｅｎｅｓｉｓ ｏｆ ＥＳＣＣ， ａｎｄ ｔｈｅ ｉｎｈｉｂｉｔｉｏｎ ｏｆ ｃｅｌｌ ｐｒｏｌｉｆｅｒａｔｉｏｎ ｉｎｄｕｃｅｄ ｂｙ ＺＮＦ７５０ ｍａｙ ｂｅ ｐａｒｔｉａｌｌｙ ｔｈｒｏｕｇｈ ｔｈｅ ｒｅｇｕｌａｔｉｏｎ ｏｆ ＫＬＦ４ ｅｘｐｒｅｓｓｉｏｎ． [ABSTRACT FROM AUTHOR]