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岭南现代临床外科 ›› 2017, Vol. 17 ›› Issue (03): 287-294.DOI: doi:10.3969/j.issn.1009?976X.2017.03.008

• 论著与临床研究 • 上一篇    下一篇

肝再生磷酸酶-3上调转化生长因子-beta促进结肠癌LoVo细胞侵袭的机制研究

施景龙 罗兴喜 许鹤洋 蓝球生 黄永亮 褚忠华   

  1. 广州市南沙区第一人民医院
  • 通讯作者: 褚忠华

Phosphatase of regenerating liver?3 promoted the invasion of LoVo cells through TGF?beta

SHI Jinglong ,LUO Xingxi ,XU Heyang ,LAN Qiusheng ,HUANG Yongliang ,CHU Zhonghua.   

  1. 1 Depart-ment of General Surgery,the First People′ s Hospital of Nansha District,Guangzhou,511440,China;2 Department of Gastroenteropancreatic Surgery ,Sun Yat?sen Memorial Hospital,Sun Yat?sen University,Guangzhou510120,China.
  • Online:2017-06-20 Published:2017-06-20
  • Contact: CHU Zhonghua

摘要:

目的 探讨转化生长因子-betaTGF?beta通路在肝再生磷酸酶?3PRL?3促进肠癌细胞侵袭和转移中的作用机方法 酶联免疫吸附试ELISA检测实验组与对照组结癌细TGF?beta水平表达差Transwell侵袭小室法检LoVo细胞侵袭能力变Westernblot检测相关通路蛋白水平变结果 ELISA实验检测结肠癌细胞转PRL?3稳定表PRL?3LoVoLoVo?P与对照LoVo?C相比TGF?beta表达明显升114±11pg/mL56±8pg/mLP<0.01Transwell侵袭实验提示不同浓度TGF?beta中和抗110100ng/mLLoVo?P后其侵袭能力逐渐降低对照组穿膜细胞数为142.11.3实验组分别为96.8.267.9.448.6.4P<0.05。蛋白印记实验提示PI3K/AKT信号通路参与了其诱导侵袭的过程使PI3K抑制剂LY29400210mg/mLLoVo?PAKT磷酸化蛋白的表达水平降2.5P<0.05结论 PRL?3能诱导结肠LoVo细胞分TGF?betaPI3K/AKT信号通路进而促进LoVo细胞侵袭

关键词: 结肠癌, 转化生长因子-beta, 肝再生磷酸酶-3, 侵袭

Abstract:

Objective To investigate role of TGF?beta in promoting the colorectal cancer LoVo cells invasion induced by phosphatase of regenerating liver-3PRL?3. Methods ELISA assay was to used to detect the level of TGF-beta in LoVo-P and LoVo-C. Invasion assays were applied to determine the effect of TGF-beta on the ability of PRL-3. Western blot was used to detect the proteins of p-AKT and AKT. Results Elisa assay displayed that the protein level of TGF?beta of LoVo?P was higher than LoVo-C 114 ± 11 pg/ml vs. 56 ± 8 pg/ml, P<0.01. When added different dosages of neutralizing antibody of TGF-beta 1, 10, 00 ng/ml in culture medium of LoVo-P, the invasion were decreased significantly96.1 ± 8.2, 67.3 ± 9.4 and 48.6 ± 6.4, respectivelyand all Pvaluesless than 0.05. Western blot reminded the proteins of p?AKT in LoVo?P were higher than LoVo?C, and the expression of p?AKT in LoVo?P was decreased by 2.5?fold after treating LoVo?P with the PI3K inhibitor LY29400210 mg/mL P<0.05. Conclusion PRL?3 could up?regulate the expression of TGF?beta in colorectal cancer LoVo cells and promote the invasion of LoVo cells, in which PI3K/AKT signaling pathway may be involved.

Key words: PRL?3, invasion, colon cancer, TGF?beta

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