microRNAs (miRNAs) are a class of endogenously expressed, small non-coding RNAs, which suppress their target mRNAs at the post-transcriptional level. miRNAs play key roles in tumor metastasis. The aim of the present study was to investigate the expression of miRNA-32 (miR-32) on the biological behavior of the human gastric cancer cell line, SGC-7901. SGC-7901 cells were transfected with miR-32-mimic, miR-32-inhibitor and empty plasmid vectors using Lipofectamine™ 2000. The expression of GFP was observed by fluorescent microscopy and miR-32 gene expression was detected by quantitative polymerase chain reaction. The cell counting kit-8 assay was performed to evaluate the effect of miR-32 expression on cell proliferation in vitro. Alterations in the migration and metastatic potential of SGC-7901 cells, prior to and following miR-32 gene transfection, were assayed by cell chemotactic migration and invasion tests. The results of the current study showed that the proliferation rate of the transfected SGC-7901 cells overexpressing miR-32 is reduced and cell chemotactic migration and invasion potentials is markedly reduced following miR-32-mimic transfection (P<0.05). In addition, the results demonstrated that overexpression of miR-32 greatly inhibits the proliferation and decreases the migration and invasion capabilities of SGC-7901 cells in vitro.

The epithelial‑to‑mesenchymal transition (EMT) has been noted as a critical event in the early step of cancer metastasis. Recent studies showed that nuclear transcription factor caudal type homeobox transcription factor 2 (CDX2) is a prognostic factor, which acts as a marker of good outcome in gastric cancer (GC) patients. However, the association between CDX2 expression and EMT has remained to be fully elucidated. The present study reported that forced overexpression of CDX2 in MKN45/CDX2 cells inhibited GC‑cell growth and proliferation, and attenuated migration and invasion in vitro. Furthermore, MKN45/CDX2 cells exhibited a significant upregulation of E‑cadherin protein and a significant downregulation of vimentin protein expression. These results were further supported by in vivo tumorigenicity assays, which showed that CDX2 suppressed gastric tumor xenograft growth and inhibited EMT in nude mice. These results indicated that CDX2 is capable of inhibiting GC‑cell growth and invasion. CDX2 may participate in the process of EMT of GC cells by regulating the expression of the epithelial and mesenchymal proteins E‑cadherin and vimentin.

RNA interference (RNAi) is an evolutionarily conserved process of gene silencing in multiple organisms, which has become a powerful tool for investigating gene function by reverse genetics. Herein, we constructed a short hairpin RNA (shRNA) lentiviral expression vector targeting a proliferation-inducing ligand (APRIL) gene in the CFPAC-1 cell (a type of cell strain of human pancreatic cancer) in order to observe the inhibitory effect of APRIL gene's shRNA on the growth of the CFPAC-1 cell in vitro and in vivo. The results showed that lentivirus-mediated RNAi effectively inhibited the expression of APRIL mRNA and protein in CFPAC-1 cells. Moreover, it can inhibit the growth of pancreatic cancer cells in vitro and in vivo. Our study indicates that lentivirus-mediated gene therapy is an attractive strategy in the treatment of pancreatic cancer and justifies the use of lentivirus in cancer gene therapy studies.

The DNA methylation inhibitor 5-aza-2′-deoxycytidine (5-aza-CdR) is widely used as an anticancer drug for the treatment of leukemia and solid tumors. Gastric cancer (GC) patients who were positive for caudal type homeobox transcription factor 2 (CDX2) expression showed a higher survival rate compared with those who were CDX2 negative, which suggests that CDX2 performs a tumor suppressor role. However, the molecular mechanisms leading to the inactivation of CDX2 remain unclear. In the present study we demonstrated that the expression levels of CDX2 and DNA methyltransferase enzyme 1 (DNMT1) mRNA were significantly higher in GC compared with distal non-cancerous tissue. The expression of CDX2 mRNA was significantly correlated with Lauren classification, TNM stage and lymph node metastasis. DNMT1 mRNA expression was significantly correlated with TNM stage, pathological differentiation and lymph node metastasis. The expression of CDX2 mRNA was inversely correlated with that of DNMT1 mRNA in GC. Hypermethylation of the CDX2 gene promoter region, extremely low expression levels of CDX2 mRNA and no expression of CDX2 protein were the characteristics observed in MKN-45 and SGC-7901 GC cell lines. Following the treatment of MKN-45 cells with 5-aza-CdR, the hypermethylated CDX2 gene promoter region was demethylated and expression of CDX2 was upregulated, while DNMT1 expression was downregulated. Furthermore, a concentration- and time-dependent growth inhibition as well as increased apoptosis were observed. Caspase-3, −8 and −9 activities increased in a concentration-dependent manner following exposure to different concentrations of 5-aza-CdR. Therefore, our data show that the overexpression of DNMT1 and methylation of the CDX2 gene promoter region is likely to be responsible for CDX2 silencing in GC. 5-Aza-CdR may effectively induce re-expression of the CDX2 gene, inhibit cell proliferation and enhance the caspase-independent apoptosis of MKN-45 cells in vitro.

Long non‑coding RNAs (lncRNAs) perform distinct biological functions by regulating gene expression through various molecular mechanisms under normal physiological and pathological conditions. However, the function of the stomach cancer‑associated transcript‑3 (STCAT3) lncRNA, including its prognostic significance and role as a binding protein in gastric cancer (GC), remain unclear. In the present study, 56 potential binding proteins of STCAT3 were screened using through mass spectrometry and bioinformatics analysis. Among these, dermcidin, GAPDH, annexin, calmodulin‑like protein, cathepsin‑D and suprabasin were demonstrated to be candidate binding proteins using a literature search. RNA‑protein interaction prediction was used to confirm these six proteins. Finally, dermcidin was identified as the binding protein of STCAT3 by comparing the mRNA and protein levels of the candidate genes and their correlations with STCAT3 in plasmid‑transfected BGC‑823 GC cell lines, as well as by validating the interplay between dermcidin and STCAT3 in other GC cell lines. Immunohistochemical analysis of tissues from 98 patients with GC further confirmed the interaction between dermcidin and STCAT3. The results of the present study also revealed that STCAT3 and dermcidin and independent predictors of overall survival in patients with GC. Furthermore STCAT3 and dermcidin are positively correlated with lymph node metastasis and tumor/node/metastasis score. In summary, the present study suggests that dermcidin is a novel binding protein of lncRNA STCAT3, which serves an important role in the progress and clinical outcome of GC.