Thus, there is an urgent need and a great clinical interest to better understand the molecular mechanisms responsible for gastric cancer metastasis in order to improve the outcome of gastric cancer patients. To this end, our recent research on gastric cancer has focused on microRNAs (miRNAs), which are small, single-stranded noncoding RNA molecules of 19–23 nucleotides in length

Tanespimycin molecular weight that are able to post-transcriptionally regulate target gene expression [6]. So far, several hundred miRNAs have been identified in plants, animals, and even viral RNA genomes. In humans, miRNAs regulate many cellular processes through binding to 3′-untranslated regions (UTRs) and other regions of protein-coding mRNA sequences of their target mRNAs to cause mRNA degradation or inhibit its translation [7]. Thus, altered miRNA expression plays a role in tumor development and progression, such as tumor cell proliferation, invasion,

and metastasis [8]; in addition, certain miRNAs also can predict the prognosis of various cancers, including gastric, breast, lung, and prostate cancers [9, 10]. In gastric cancer, aberrant expression of miRNAs has been linked to tumor metastasis; for example, plasma levels of miR-223, miR-21, miR-218, and miR-25 have been linked to gastric cancer metastasis [11, 12]. Furthermore, elevated miR-21 expression is associated with lymph node metastasis Buparlisib of gastric cancer [13]. Thus, these miRNAs could be useful as biomarkers to predict gastric cancer lymph node metastasis. In addition, miR-625 expression is significantly downregulated

and inversely associated with lymph node metastasis of gastric cancer [14]. Therefore, in the present study, we first performed miRNA array analysis to profile differentially expressed miRNAs between primary and secondary gastric cancer tissues. We found that the expression of hsa-miR-134 and hsa-miR-337-3p was significantly less in metastatic lymph node tissues than in primary tumors of gastric cancer. Next, we Gemcitabine investigated the effects of hsa-miR-134 or hsa-miR-337-3p on the inhibition of gastric cancer cell growth and invasion. The results of this study may be useful to find potential therapeutic agents to inhibit gastric cancer metastasis. Methods Tissue samples In this study, samples of human primary gastric cancer and the corresponding metastatic lymph node tissues were collected from 19 patients and stored in liquid nitrogen until use. The demographic data of these patients are shown in Table 1. The institutional review board of the First Affiliated Hospital of Bengbu Medical College approved our protocol, and the patients signed a consent form to participate in this study.