Frequently rearranged in advanced T cell lymphomas-1 (FRAT1) positively regulates the Wnt/β-catenin signaling pathway by inhibiting glycogen synthase kinase-3 mediated phosphorylation of β-catenin. FRAT1 is a proto-oncogene, implicated in tumorigenesis. The present study aimed to investigate the effects of FRAT1 silencing on the proliferation and apoptosis of SGC7901 cells. FRAT1 in SGC7901 cells was silenced by RNA interference. Reverse transcription-quantitative polymerase chain reaction was used for the analysis of FRAT1 mRNA and western blotting was used to evaluate FRAT1 and β-catenin protein levels. Cell proliferation was analyzed by the MTT assay. Cell cycle distribution and apoptosis were analyzed by flow cytometry. The expression of FRAT1 mRNA, FRAT1 and β-catenin protein in FRAT1-silenced SGC7901 cells were reduced significantly compared to untreated cells. The proliferation of FRAT1 silenced SGC7901 cells decreased significantly The FRAT1 silenced SGC7901 cells were arrested at G0/G1 stage to a greater degree, and apoptosis was increased. In summary, silencing of FRAT1 inhibits SGC7901 cell proliferation and induces apoptosis, possible through a reduction in β-catenin expression. FRAT1 may serve as a prognostic biomarker and therapeutic target for gastric cancer.

The metastatic behavior of hepatocellular carcinoma (HCC) is one of the key factors that leads to poor prognosis. The aim of the current study was to determine the changes in metastasis and the proliferation potential of bone marrow mesenchymal stem cells (BMSCs) in high metastatic potential hepatocellular carcinoma (MHCC97-H) following gene silencing. The osteopontin (OPN) and transforming growth factor-β (TGFβ 1) genes, which are associated with metastasis and tumor proliferation, were silenced in MHCC97-H cells. Transwell assays were used to evaluate the migration of MHCC97-H cells in vitro. Additionally, a murine model of MHCC97-H lung metastasis was established. Following OPN and TGFβ 1 silencing, the migration of MHCC97-H cells was significantly reduced following BMSC intervention (P<0.01). Furthermore, there were few MHCC97-H cells in the lung tissues of the OPN-and TGFβ 1-silenced animals, and their integrated optical density (IOD) value was significantly lower compared with controls (P<0.05). Immunofluorescence of lung metastasis in the MHCC97-H model revealed that there was no significant difference in the IOD value of integrin α v β 3 expression in the OPN-and TGFβ 1-silenced groups compared with controls (P>0.05). The metastasis and proliferation potential of MHCC97-H following BMSC intervention were significantly reduced in vitro and in vivo, especially in the TGFβ 1-silenced group. The decrease in the metastatic potential in gene-silenced MHCC97-H cells was not associated with integrin α v β 3 expression. Therefore, OPN and TGFβ 1 may be potential targets for HCC treatment, and TGFβ 1 may have a higher therapeutic potential for BMSC intervention.