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The Mechanisms of Inhibiting the Migration in Human Gastric Cancer Cells Induced by Rosiglitazone

Author: LiuCan
Tutor: ChenHongHui
School: Nanhua University
Course: Department of Gastroenterology,
Keywords: Migrate Rosiglitazone Rac1 Rock Pak1 LIMK1 cofilin - 1
CLC: R735.2
Type: Master's thesis
Year: 2011
Downloads: 36
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Abstract

Background and purpose of rosiglitazone (Rosiglitazone ROS) on a variety of tumor cells significantly inhibited, is a great value for development of anti-tumor drug candidate. In recent years, the significance of LIMK1 in tumorigenesis has attracted wide attention. LIMK1 plays an important role in regulating tumor cell migration, it may be one of the key molecules that cause tumor cell metastasis. Rosiglitazone specific anti-tumor mechanism of action is unclear. The purpose of this study is to investigate the impact of rosiglitazone on the expression of signaling pathways in human gastric cancer the the SGC7901 and SGC7901/VCR cells LIMK1, to clarify the molecular mechanism of anti-tumor cell migration and metastasis. [Method] The scratch test rosiglitazone ability to influence cell migration. RT-PCR the detection SGC7901 cells and SGC7901/VCR of cells Rac1, Rock, PAK1, of LIMK1 and cofilin-1 mRNA expression; Western blot detection of the SGC7901 cells and SGC7901/VCR cells Rac1, Rock, PAK1, of LIMK1 and cofilin-1 protein expression. [Results]. Rosiglitazone on human gastric cancer SGC7901 the cells and SGC7901/VCR cell migration scratches experimental observation of rosiglitazone on cell migration. The results showed that 40 mg · L-1 rosiglitazone respectively role SGC7901 cells and SGC7901/VCR cells after 24 h, inhibition of cell migration. 2 of rosiglitazone on phosphorylation of cofilin ^{-1 of RT-PCR and Western blot results showed that rosiglitazone (40 mg · L ^{-1 ) no effect on SGC7901 and SGC7901/VCR are cells cofilin ^{-1 expression, Western blot showed that the role of rosiglitazone (40 mg · L ^{-1 ) SGC7901 and SGC7901 / VCR cells after 24 h, the cells P-cofilin ^{-1 expression levels of decline, suggesting that the cells cofilin ^{-1 phosphorylation levels decreased, indicating that rosiglitazone inhibited SGC7901 SGC7901 / VCR the cells in cofilin ^{-1 activity. 3 of rosiglitazone on human gastric cancer SGC7901 and SGC7901/VCR cells LIMK1 expression affect the RT-PCR results showed that 40 mg · L ^{-1 rosiglitazone and role of SGC7901 and SGC7901/VCR cells 24h after the cells LIMIK1 mRNA levels were significantly suppressed. Western blot analysis showed that 40 mg · L ^{-1 rosiglitazone and SGC7901 and role of SGC7901/VCR cells for 24 h, cells LIMK1 protein expression levels decline. 4. Rosiglitazone the Rac1/Rock/Pak1 pathway affect the RT-PCR showed that rosiglitazone (40 mg · L ^{-1 ) for 24h, cell Rac1mRNA, RockmRNA and Pak1mRNA expression levels. Western blot showed that the role of rosiglitazone (40 mg · L ^{-1 ) SGC7901 and SGC7901/VCR cells after 24 inhibited of RAc1 ??of cells, Rock and Pak1 protein. [Conclusion] 1. Rosiglitazone on human gastric cancer SGC7901 and SGC7901/VCR cell migration inhibition. Rosiglitazone anti-tumor cell migration transfer mechanism may-Pak1 pathway by blocking the Rac1-Rock from the down-regulation of LIMK1 expression and thus inhibit the activation of cofilin ^{-1 .}}}}}}}}}}}}

The Mechanisms of Inhibiting the Migration in Human Gastric Cancer Cells Induced by Rosiglitazone

Abstract

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