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目的观察GLUD1对结直肠癌细胞侵袭和迁移能力的影响,探讨其可能的分子机制。方法采用慢病毒转染下调GLUD1的表达,Transwell侵袭实验检测sh GLUD1对肠癌细胞Lovo和SW480侵袭能力的影响,划痕实验检测sh GLUD1对Lovo和SW480迁移能力的影响,Western blot检测GLUD1和AG490对E-cadherin、Vimentin、ZEB1、STAT3及p STAT3表达的影响。结果慢病毒转染sh GLUD1可显著下调GLUD1在结肠癌细胞中的表达;下调GLUD1的表达可抑制结肠癌细胞Lovo和SW480的侵袭迁移能力;GLUD1可促进STAT3磷酸化,以及上调Vimentin、ZEB1和下调E-cadherin的表达;而AG490处理则可抑制STAT3的磷酸化,上调Ecadherin和下调Vimentin、ZEB1的表达。结论 GLUD1可通过活化STAT3信号调控上皮间质转化(EMT),进而促进结肠癌细胞的侵袭迁移能力。
Objective To observe the effect of GLUD1 on invasion and migration of colorectal cancer cells and to explore its possible molecular mechanism. Methods The expression of GLUD1 was down-regulated by lentivirus transfection, the effect of sh GLUD1 on invasion ability of Lovo and SW480 cells was detected by Transwell invasion assay, the effect of sh GLUD1 on the migration of Lovo and SW480 was detected by scratch assay, the GLUD1 and AG490 On E-cadherin, Vimentin, ZEB1, STAT3 and p STAT3 expression. Results Lentiviral transfection of sh GLUD1 significantly down-regulated the expression of GLUD1 in colon cancer cells. Down-regulation of GLUD1 inhibited the invasion and migration of colon cancer cells Lovo and SW480. GLUD1 promoted phosphorylation of STAT3 and up-regulated Vimentin and ZEB1 E-cadherin. However, AG490 inhibited the phosphorylation of STAT3, up-regulated Ecadherin and down-regulated the expression of Vimentin and ZEB1. Conclusion GLUD1 can regulate epithelial-to-mesenchymal transition (EMT) through activation of STAT3 signaling, thereby promoting invasion and migration of colon cancer cells.