In contrast, expression of hsa-miR-337-3p was only detected in th

In contrast, expression of hsa-miR-337-3p was only detected in three gastric cancer cell lines, i.e., SNU-5, HGC27, and SGC-7901, at a low level (Figure 2B). Figure 2 Expression of hsa-miR-134 and hsa-miR-337-3p in the nonmalignant gastric cell line GES and nine gastric

cancer cell lines. A, hsa-miR-134; B, hsa-miR-337-3p. Effect of selleck products mimics and inhibitors of hsa-miR-134 and hsa-miR-337-3p on MKN-45 cell proliferation To determine the effects of hsa-miR-134 and hsa-miR-337-3p on the regulation of gastric cancer growth and invasion, we selected the MKN-45 cell line according to its expression levels of these two miRNAs. The mimic was used to determine whether overexpression Daporinad supplier of these two miRNAs could inhibit tumor cell invasion in vitro, whereas inhibitors were used as controls. (Although they were downregulated in gastric tumor cells, they may have certain levels of expression in tumor cells, and inhibition of their expression may ALK targets also promote tumor cell invasion.) We transfected hsa-miR-134 or hsa-miR-337-3p mimics or inhibitors into MKN-45 cells and performed a cell viability assay. The data revealed that the changed expression of hsa-miR-134 or hsa-miR-337-3p only slightly affected MKN-45 cell proliferation (Figure 3). miRNA mimics and inhibitors used in this study were listed in Additional file 3: Table S2. Figure 3 Time-course effects of miRNAs on the regulation

of gastric cancer MKN-45 cell proliferation. SPTLC1 A, hsa-miR-337-3p mimic-transfected MKN-45 cells. B, hsa-miR-134 inhibitor-transfected MKN-45 cells. Data are expressed as mean ± SD; n=4. Expression of hsa-miR-337-3p affects MKN-45 cell migration and invasion Since these miRNAs were differentially expressed in primary and secondary gastric cancer tissues, we investigated the effects of hsa-miR-134 and hsa-miR-337-3p on

the regulation of gastric cancer cell migration by transfecting hsa-miR-134 and hsa-miR-337-3p mimics or inhibitors into MKN-45 cells and then measured the tumor cell migration capacity. Next, the capacity of the transfected cells was examined using a Transwell-Matrigel invasion assay. Our data showed that transfection with the hsa-miR-134 mimic or inhibitor in MKN-45 cells did not affect the tumor cell invasion capacity (Figure 4A; P>0.05). In contrast, the hsa-miR-337-3p mimic significantly decreased the number of invaded cells (Figure 4B; P<0.05), indicating that hsa-miR-337-3p overexpression may decrease the invasive ability of gastric cancer cells. Figure 4 The effect of hsa-miR-337-3p or hsa-miR-134 mimics or inhibitors on the regulation of gastric cancer cell invasive capacity. A, The migrated cell number of the hsa-miR-134 inhibitor-transfected MNK-45 cells; B: The migrated cell number of the hsa-miR-337-3p mimic-transfected MNK-45 cells. Data are expressed as mean ± SD; n=4; *P<0.05, as compared to the control oligonucleotide (NC) treated group.

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