The aim of this study was to investigate the effects of small interfering RNA (siRNA) targeting human growth hormone receptor (hGHR) combined with 5-fluorouracil (5-FU) on the hepatic metastasis of colon cancer. The animal model of liver metastases using human SW480 colon cancer cells was established on BALB/c mice and the siRNA interfering plasmid targeting hGHR gene was constructed. The tumor-bearing mice were randomly divided into the saline control, plasmid, growth hormone (GH), 5-FU, 5-FU+plasmid and 5-FU+plasmid+GH groups. The liver metastasis in each group was observed. All the animals showed liver metastases and using siRNA-interfering plasmid treatment the incidence of liver metastases was significantly reduced in the tumor groups compared to the saline or GH group. The combined treatment of interfering plasmid and 5-FU slightly decreased the incidence of liver metastases in the tumor groups compared to the plasmid alone or 5-FU alone treatment, although the findings were not statistically significant. On the basis of the combination of interfering plasmid and 5-FU, the additional GH did not increase the incidence of liver metastases (P>0.05), but improved the weight loss of the mice (P<0.05) induced by the inhibition of GHR and toxicity of 5-FU. The present results showed that siRNA targeting hGHR is able to reduce the incidence of liver metastases of human SW480 colon cancer cells in mice. Thus, GHR may be important in tumor metastasis.

Glioma is a common malignacy of the brain that affects elderly patients in particular. Despite treatment, however, the survival rate is 12 months. The aim of the present study was to examine the therapeutic effect of neural progenitor cells (NPCs) on a glioma murine model, and to determine the possible mechanism of action. A glioma murine model was constructed and the tumor volume and tumor growth rate were measured. The therapeutic effect of cell injection on the glioma mouse model mice was confirmed. The quantitative polymerase chain reaction method was used to detect the expression of proto-oncogene and tumor suppressor gene. Intracranial injection of NPCs was performed to determine cell apoptosis. Preliminary results showed the mechanism of cell therapy effect at the transcription and cellular level. Compared with the model group, the tumor volume of the mice of the cell therapy group was significantly reduced from the 6th to 8th week, and the tumor growth rate was downregulated. The mechanism of action identified that NPCs regulate gene expression in tumor tissues, increase the expression of tumor suppressor gene, downregulate the gene expression of tumor cells, and reverse the proto-oncogene and imbalance of gene expression in gliomas. In conclusion, the new type of cell injection method can regulate the proto-oncogene of tumor tissue and tumor suppressor gene, improve the function phenotype of the cell, and effectively improve the clinical symptoms of mice with gliomas.

Background. There is a significant role for peroxisome proliferator-activated receptors (PPARs) in the development of cancer. Nevertheless, the role of PPARs-related genes in ovarian cancer (OC) remains unclear. Methods. The open-accessed data used for analysis were downloaded from The Cancer Genome Atlas database, which was analyzed using the R software. Results. In our study, we comprehensively investigated the PPAR target genes in OC, including their biological role. Meanwhile, a prognosis signature consisting of eight PPAR target genes was established, including apolipoprotein A-V, UDP glucuronosyltransferase 2 family, polypeptide B4, TSC22 domain family, member 1, growth hormone inducible transmembrane protein, renin, dedicator of cytokinesis 4, enoyl CoA hydratase 1, peroxisomal (ECH1), and angiopoietin-like 4, which showed a good prediction efficiency. A nomogram was constructed by combining the clinical feature and risk score. Immune infiltration and biological enrichment analysis were applied to investigate the difference between high- and low-risk patients. Immunotherapy analysis indicated that low-risk patients might respond better to immunotherapy. Drug sensitivity analysis indicated that high-risk patients might respond better to bleomycin, nilotinib, pazopanib, pyrimethamine, and vinorelbine, yet worse to cisplatin and gefitinib. Furthermore, the gene ECH1 was selected for further analysis. Conclusions. Our study identified a prognosis signature that could effectively indicates patients survival. Meanwhile, our study can provide the direction for future studies focused on the PPARs in OC.