Our data should be more biologically representive because of the larger numbers of clinical samples. Only a greater part but not all of the GC patients have a down-regulation of miR-10a in their GC tissues although miR-10a functions as a tumor suppressor in gastric cancer cells. This may be because of distinct mechanism of the genesis of GC in different individuals. There might be some other important genes or factors responsible for tumorigenesis in the GC patients in whose GC tissues miR-10a was unchanged or up-regulated. In addition, the miR-10a expression exhibited no correlation with clinicopathological characteristics except for TNM stage, indicating that miR-10a might play a partial role in tumorigenesis especially in early stages. Many miRNAs have been reported to correlate with tumorigenesis, however, the underlying molecular mechanism remains unclear. In our report, a functional analysis of miR-10a, including cell proliferation, migration and invasion assays, helped us to better understand the contribution of miR-10a to gastric carcinogenesis. Indicating that the repression of miR-10a might promote tumor progression in gastric carcinogenesis. Future studies are needed to elucidate this mechanism. In the human genome, miR-10a is located upstream of HOXB4. MiR-10b, another member of the miR-10 family, is located upstream of HOXD4. These two members are different from each other in only one base and ICG-001 exhibit identical seed sequences, suggesting their similar functions. Kwoneel Kim has reported that miR-10b plays a role in GC as a tumor suppressor. In our study, we demonstrated that the overexpression of miR-10a inhibited tumor proliferation, migration and invasiveness, which was similar to the function of miR-10b in GC. HOX genes are highly conserved transcription factors that are determinant for correct anterior-posterior patterning of the body axis. HOXA1 has been validated as a direct target of miR-10a in human pancreatic cancer and megakaryocytopoiesis. We also observed that the overexpression of miR-10a decreased HOXA1 protein levels in two GC cell lines, suggesting that HOXA1 is a direct target of miR-10a in gastric cancer. Epigenetic modifications have been shown to be key mediators underlying the down-regulation of miRNA expression and exhibit a tight correlation with carcinogenesis. Our data demonstrated that the hypermethylation of the CpG island upstream of miR-10a led to the down-regulation of miR-10a in GC cell lines and GC patients. Moreover, AZA treatment increased miR-10a in GC cell lines. Based on our findings, the methylation status of miR-10a may be employed as a potential biomarker in GC. In summary, this study reports that miR-10a acts as a tumor suppressor in GC cells and is partly down-regulated by DNA hypermethylation. Forced expression of miR-10a suppresses cell proliferation, migration and invasiveness in vitro. The methylation status and the expression level of miR-10a may serve as potential biomarkers of GC, and miR-10a may have potential therapeutic value in cancer therapy.