Tichostatin A inhibiting migration and invasion of human gastric carcinoma SGC-7901 cells via up-regulating protocadherin 9 / 解剖学报

ABSTRACT

Objective To investigate the effect of trichostatin A (TSA) on migration and invasion in human gastric carcinoma SGC-7901 cells and its possible mechanism. Methods SGC-7901 cells were cultured in vitro and treated with TSA (5, 10, 20, 40, 80, 160 nmol/L) for 48 hours, and then the cell viability was detected by cell counting kit 8 (CCK-8) assay. The protocadherin 9 (PCDH9) high-expression SGC-7901 cells were stably established by transfecting with eukaryotic expression vector (pCMV6-PCDH9). Transwell assay was used to determine the abilities of migration and invasion. The mRNA expression level of PCDH9 were measured by RT-PCR. Western blotting was performed to analyze the protein expression of PCDH9, Snail, E-cadherin, matrix metalloproteinase (MMP)-2 and MMP-9. Results TSA remarkably reduced the cell viability of SGC-7901 cells in excess of 80 nmol/L (P<0. 05). However, in a dose-dependent manner, low-level TSA (5-20 nmol/L) suppressed migration and invasion of SGC-7901 cells (P<0. 05), down-regulated the protein levels of Snail, MMP-2 and MMP-9 (P<0. 05), and up-regulated the protein levels of PCDH9 and E-cadherin (P<0. 05). Meanwhile, high expression of PCDH9 also inhibited migration and invasion of SGC-7901 cells (P<0. 05), down-regulated the protein levels of Snail, MMP-2 and MMP-9 (P<0. 05), and up-regulated the protein level of E-cadherin (P<0. 05). Conclusion TSA may inhibit migration and invasion of SGC-7901 cells most likely via up-regulating PCDH9, and then down-regulating the protein levels of Snail, MMP-2 and MMP-9, and up-regulating the protein level of E-cadherin.