Dextran sulfate inhibition on human gastric cancer cells invasion, migration and epithelial-mesenchymal transformation

摘要

The objective of the present study was to observe the influence of dextran sulfate (DS) on the proliferation, invasion and migration of AGS, BGC-23, GES-1, MGC-803 and SGC-7901 cells. Additionally, the possible inhibition mechanism of DS on BGC-823 cells epithelial-mesenchymal transition (EMT) was explored. The cells in the control and experimental group were treated with PBS and DS respectively. The effect of DS on the invasion and migration of these five types of cells were investigated using Transwell invasion and migration assays. Immunocytochemistry, western blotting and reverse transcription-polymerase chain reaction (RT-PCR) assays were used to measure gene and protein expression of hypoxia-inducible factor 1 (HIF1-a) and EMT associated factors [Twist, E-cadherin, N-cadherin and -catenin] of BGC-823 cells. According to the results of CCK-8, DS significantly decreased the proliferation of AGS, SGC-7901 and BGC-823 cells to different extents, but there were no notable differences for MGC-803 cells. Transwell migration and invasion results demonstrated that, compared with the control group, DS reduced the migration and invasion of every types of cells to different extents, and the inhibition to BGC-823 cells invasion is the most notably. Immunofluorescence, RT-PCR and western blot analysis results indicated that HIF-1, Twist and N-cad expressions levels had different degrees of reduction in the experimental group following DS treatment; however, the expression level of E-cad had increased. In conclusion, DS inhibited the proliferation of AGS, BGC-823, SGC-7901 and GES-1 cells, the inhibition degree may be associated with the differentiation degree of every cancer cell, the higher the differentiation degree, the stronger the inhibition. DS inhibited migration and invasion of the five types of gastric cancer cells in different degree. DS may inhibit EMT of BGC-823 by inhibiting Wnt signaling.