agar and Osteosarcoma

Primary bone cancers commonly involve surgery to remove the malignant tumor, complemented with a postoperative treatment to prevent cancer resurgence. Studies on magnetic hyperthermia, used as a single treatment or in synergy with chemo- or radiotherapy, have shown remarkable success in the past few decades. Multifunctional biomaterials with bone healing ability coupled with hyperthermia property could thus be of great interest to repair critical bone defects resulting from tumor resection. For this purpose, we designed superparamagnetic and bioactive nanoparticles (NPs) based on iron oxide cores (γ-Fe

Topics: Agar; Biocompatible Materials; Bone Neoplasms; Glass; Humans; Hyperthermia, Induced; Magnetic Phenomena; Osteosarcoma; Silicon Dioxide

Zinc finger X-chromosomal protein (ZFX) is a member of the zinc finger family of proteins. The importance of ZFX in several cancer types, including prostate cancer, laryngeal squamous cell carcinoma, and glioma, has been addressed. However, the role of ZFX in human osteosarcoma remains unknown. Here we investigated the phenotype of ZFX knockdown on cell proliferation and in vitro tumorigenesis using lentivirus-mediated loss-of-function strategy. The results demonstrated that the proliferation and colony formation ability of human osteosarcoma Saos-2 and MG63 cells was impaired by ZFX small interfering RNA (siRNA)-expressing lentivirus. Moreover, loss of ZFX led to G0/G1 phase cell cycle arrest and a significant increase of cells in the sub-G1 fraction, indicating that ZFX functions as an oncogene in the malignant proliferation process in osteosarcoma. Furthermore, ZFX siRNA may have an antitumorigenic effect on osteosarcoma cells. Our findings hold important significance for RNA interference-mediated cancer gene therapy for human osteosarcoma.

Topics: Agar; Apoptosis; Bone Neoplasms; Carcinogenesis; Cell Culture Techniques; Cell Growth Processes; Down-Regulation; Gene Knockdown Techniques; Humans; Kruppel-Like Transcription Factors; Osteosarcoma; RNA, Small Interfering; Zinc Fingers

hTid-1, a human homolog of the Drosophila tumor suppressor l(2)Tid and a novel DnaJ protein, regulates the activity of nuclear factor kappaB (NF-kappaB), but its mechanism is not established. We report here that hTid-1 strongly associated with the cytoplasmic protein complex of NF-kappaB-IkappaB through direct interaction with IkappaBalpha/beta and the IKKalpha/beta subunits of the IkappaB kinase complex. These interactions resulted in suppression of the IKK activity in a J-domain-dependent fashion and led to the cytoplasmic retention and enhanced stability of IkappaB. Overexpression of hTid-1 by using recombinant baculovirus or adenovirus led to inhibition of cell proliferation and induction of apoptosis of human osteosarcoma cells regardless of the p53 expression status. Adherent cultured cells transduced with Ad.hTid-1 detached from the dish surface. Morphological changes consistent with apoptosis and cell death were evident 48 h after Ad.EGFP-hTid-1 transduction. In contrast, cells transduced with Ad.EGFP or Ad.EGFP-hTd-1DeltaN100, a mutant that has the N-terminal J domain deletion and that lost suppressive activity on IKK, continued to proliferate. Similar data were obtained with A375 human melanoma cells. Ad.EGFP or Ad.EGFP-hTd-1DeltaN100 ex vivo-transduced A375 cells injected subcutaneously into nude mice produced growing tumors, whereas Ad.EGFP-hTid-1-transduced cells did not. Collectively, the data suggest that hTid-1 represses the activity of NF-kappaB through physical and functional interactions with the IKK complex and IkappaB and, in doing so, it modulates cell growth and death.

Topics: Adenoviridae; Agar; Animals; Apoptosis; Baculoviridae; Cell Death; Cell Line; Cell Line, Tumor; Cell Proliferation; Cytoplasm; Drosophila; Gene Deletion; Gene Expression Regulation; Genes, Reporter; Glutathione Transferase; Green Fluorescent Proteins; Heat-Shock Proteins; HSP40 Heat-Shock Proteins; Humans; I-kappa B Proteins; Immunoprecipitation; Lentivirus; Male; Mice; Mice, Nude; Microscopy, Fluorescence; Mutation; Neoplasm Transplantation; NF-kappa B; Osteosarcoma; Plasmids; Protein Binding; Protein Structure, Tertiary; Recombinant Fusion Proteins; Signal Transduction; Tetrazolium Salts; Thiazoles; Time Factors; Transfection; Tumor Suppressor Protein p53

The TE-85 osteosarcoma cell line has several of the in vitro properties of malignant cells, including colony formation in agar, but has low extracellular fibrinolytic activity and no capacity to form tumors in ATS-treated hamsters. Some TE-85 cells clones (clones 2, 4 and 6) have increased fibrinolytic activity but do not form tumors in hamsters. TE-85 cells infected with mammalian transformation-defective viruses have low (FeLV) or increased (RD-114 virus) levels of fibrinolytic activity and do not form tumors in hamsters. TE-85 cell either nonproductively infected with Ki-MSV or productively infected with M-MSV (RD-114), have fibrinolytic activity and can form tumors in hamsters. The MSV gene(s) but not colony formation in agar or extracellular fibrinolytic activity appears to be capable of rendering TE-85 cells tumorigenic in ATS-treated hamsters.

Topics: Agar; Animals; Antilymphocyte Serum; Cell Line; Cell Transformation, Neoplastic; Clone Cells; Cricetinae; Culture Media; Fibrinolysis; Humans; Immunosuppression Therapy; In Vitro Techniques; Neoplasm Transplantation; Neoplasms, Experimental; Oncogenic Viruses; Osteosarcoma; T-Lymphocytes; Transplantation, Heterologous

Topics: Adolescent; Adult; Agar; Bone Neoplasms; Child; Culture Techniques; Electrophoresis; Female; Fetus; Gels; Giant Cell Tumors; Humans; Isoenzymes; L-Lactate Dehydrogenase; Male; Middle Aged; Osteosarcoma; Pregnancy