Titanium dioxide nanoparticles (nano-TiO2) are manufactured and used worldwide in large quantities. However, phytotoxicity research on nano-TiO2 has yielded confusing results, ranging from strong toxicity to positive effects. Therefore, in this research, the effects of nano-TiO2 on the germination and root elongation of seed and seedlings were studied. Additionally, the uptake and physiological responses of mature plants were investigated. Physical chemistry data were analyzed to assess the availability of nano-TiO2. Finally, a hydroponic system designed to overcome nano-TiO2 precipitation was used to reproduce the environmental conditions of actual fields. Nano-TiO2 did not have any effect on seed germination or on most of the plant species tested. Nano-TiO2 had positive effects on root elongation in some species. No physiological differences in enzyme activities or chlorophyll content were detected, even though the plants absorbed nano-TiO2. Physical chemistry data showed that nano-TiO2 agglomerated rapidly and formed particles with much bigger hydrodynamic diameters, even in distilled water and especially in a hydroponic system. Furthermore, agglomerated nano-TiO2 formed precipitates; this would be more severe in an actual field. Consequently, nano-TiO2 would not be also readily available to plants and would not cause any significant effects on plants. Our results and other reports suggest that titanium itself is not phytotoxic, even though plants absorb titanium. In conclusion, nano-TiO2 is not toxic to the three plant species, in vitro or in situ.

No abstract

No abstract

NANOG, a stemness-associated transcription factor, is highly expressed in many cancers and plays a critical role in regulating tumorigenicity. Transformation/transcription domain-associated protein (TRRAP) has been reported to stimulate the tumorigenic potential of cancer cells and induce the gene transcription of NANOG. This study aimed to investigate the role of the TRRAP-NANOG signaling pathway in the tumorigenicity of cancer stem cells. We found that TRRAP overexpression specifically increases NANOG protein stability by interfering with NANOG ubiquitination mediated by FBXW8, an E3 ubiquitin ligase. Mapping of NANOG-binding sites using deletion mutants of TRRAP revealed that a domain of TRRAP (amino acids 1898–2400) is responsible for binding to NANOG and that the overexpression of this TRRAP domain abrogated the FBXW8-mediated ubiquitination of NANOG. TRRAP knockdown decreased the expression of CD44, a cancer stem cell marker, and increased the expression of P53, a tumor suppressor gene, in HCT-15 colon cancer cells. TRRAP depletion attenuated spheroid-forming ability and cisplatin resistance in HCT-15 cells, which could be rescued by NANOG overexpression. Furthermore, TRRAP knockdown significantly reduced tumor growth in a murine xenograft transplantation model, which could be reversed by NANOG overexpression. Together, these results suggest that TRRAP plays a pivotal role in the regulation of the tumorigenic potential of colon cancer cells by modulating NANOG protein stability.