MicroRNA-137 is downregulated in human osteosarcoma and regulates cell proliferation and migration through targeting FXYD6.

BACKGROUND: In this work, we investigated the functional role of microRNA 137 (miR-137) in regulating osteosarcoma both in vitro and in vivo. METHODS: Quantitative RT-PCR was used to examine the gene expressions of miR-137 in osteosarcoma cell lines and osteosarcoma tumors. 143B and Saos-2 cells were infected with lentivirus expressing miR-137 mimics (miR-137-mimic) to ectopically upregulate miR-137. In vitro cancer proliferation and migration were examined by MTT assay and transwell assay, respectively. Viral infected Saos-2 cells were also subcutaneously inoculated into null mice to evaluate the effect of miR-137 upregulation on in vivo tumor growth. The interaction between miR-137 and its downstream target, FXYD6, was evaluated by dual-luciferase reporter assay and quantitative real-time PCR. FXYD6 was then subsequently upregulated in osteosarcoma cells to evaluate its effect on miR-137 regulation in osteosarcoma. RESULTS: We found that miR-137 was significantly downregulated in both osteosarcoma cell lines and osteosarcoma tumors. Lentiviral infection of miR-137-mimic upregulated miR-137 gene expression, reduced in vitro proliferation and migration and inhibited in vivo osteosarcoma tumor growth. FXYD6 was verified to be directly interacting with miR-137, and its subsequent upregulation reversed the inhibitory effect of miR-137 upregulation in osteosarcoma. CONCLUSION: We revealed novel functional role of miR-137 in osteosarcoma regulation, likely through FXYD6 binding.

Sphere-forming tumor cells possess stem-like properties in human fibrosarcoma primary tumors and cell lines.

Fibrosarcoma is a malignant soft tissue tumor of mesenchymal origin. Despite advances in medical and surgical treatment, patient survival rates have remained poor. According to the cancer stem cell hypothesis, tumors are comprised of heterogeneous cell populations that have different roles in tumor formation and growth. Cancer stem cells are a small cell subpopulation that exhibits stem-like properties to gain aggressiveness and recurrence. These cells have been identified in a variety of cancerous tumors, but not in human fibrosarcoma. In this study, we observed that HT1080 cells and primary fibrosarcoma cells formed spheres and showed higher self-renewal capacity, invasiveness and drug resistance compared with their adherent counterparts. Moreover, we demonstrated that the cells showed higher expression of the embryonic stem cell-related genes Nanog, Oct3/4, Sox2, Sox10 and their encoding proteins, as well as greater tumorigenic capacity in nude mice. In conclusion, our data suggest the presence of a stem-like cell population in human fibrosarcoma tumors, which provides more evidence for the cancer stem cell hypothesis and assistance in designing new therapeutic strategies against human fibrosarcoma.

Respiratory viruses in hospitalized children with acute lower respiratory tract infections in harbin, China.

This study investigated the prevalence of respiratory viruses, including respiratory syncytial virus (RSV), influenza virus types A and B (Flu A/B), parainfluenza virus (Para) 1-3, and adenovirus (Ad), in hospitalized children with acute lower respiratory tract infections (ALRIs). Immunofluorescence assays identified viral etiology in 412 patients younger than 16 years old. The overall viral isolation rate was 63.1% (260/412). The RSV was detected in 25.0%, Flu A/B in 19.4%, Para 1-3 in 14.6%, and Ad in 4.1% of the total sample. Multiple viruses were detected in 6.6% of the study population. Most viral infections occurred in the first 5 years of life, and the incidence of viral infection peaked during early spring and winter. Infection with Ad often resulted in the development of severe pneumonia in older children, and during the summer. The sequences of the isolated Ad hexons belonged to species B, and were closely related to the Gomen strain isolated in the United States in the 1950s. The study results will help determine the etiologic agents of ALRI in children and establish prevention and treatment programs.