The viability of A549 cells, a human lung carcinoma epithelial cell line, was evaluated after exposure to graphene oxide (GO) and its derivatives (dodecylamine GO (DA-GO), reduced GO (rGO), and sodium dodecyl sulfate rGO (SDS-rGO)). A decrease in the relative amounts of C-OH bonds and an increase in the number of C-C and C-N bonds in the C 1s spectra indicated that the reduction of GO to rGO and the surface functionalization of GO has taken place. The appearance of amine stretching bands, out-of-plane C-H stretching vibrations, and S = O stretching bands in the infrared spectra indicated the formation of DA-GO, rGO, and SDS-rGO, respectively. Low concentrations (3-25 µg/mL) of GO, rGO, and SDS-rGO were found to be mildly toxic, whereas DA-GO exhibited severe dose-dependent toxicity over the same concentration range. High concen- trations (50-400 µg/mL) of GO and all its derivatives resulted in severe toxicity to the A549 cells. It is believed that surface functionality strongly affects the viability of A549 cells.
This study investigated cytotoxicity, particularly autophagy, in RAW264.7 cells exposed to graphene oxide (GO) and its derivatives (dodecylamine-GO (DA-GO), reduced GO (rGO), and sodium dodecyl sulfate-rGO (SDS-rGO)). Appearance of amine stretching bands, out-of-plane C-H stretching vibrations, and S=O stretching bands in infrared spectra indicated the formation of DA-GO, rGO, and SDS-rGO, respectively. Light microscopy and microculture tetrazolium assay showed that all the GO types exerted cytotoxic effects on RAW264.7 cells in a concentration-dependent manner. Higher concentrations of the GO types downregulated the expression of PU.1, a unique transcription factor in monocytes and macrophages, and decreased the conversion of LC3A/B-I to LC3A/B-II, suggesting that PU.1 was associated with autophagy in RAW264.7 cells. These results suggested that surface-functionalized GOs exerted cytotoxic effects in a concentration-dependent manner by changing the expression of critical genes and inducing autophagy in macrophages.
death in China and worldwide. Due to the difficulty in early diagnosis and the onset of cancer metastasis, the 5-year survival rate of lung cancer remains extremely low. JAK2 has emerged as pivotal participant in biological processes, often dysregulated in a range of cancers, including lung cancer. Recently we found that JAK2 might play an important role in lung cancer pathogenesis as an oncogene. While our understanding of JAK2 in the onset and progression of lung cancer is still in its infancy, there is no doubt that understanding the activities of JAK2 will certainly secure strong biomarkers and improve treatment options for lung cancer patients. Methods: The expression levels of JAK2 mRNA and protein were assayed using the RT-PCR and Western Blot assay respectively. MTT assay, Scratch-wound healing assay, Transwell migration and invasion assay were conducted to study the proliferation, migration and invasion abilities of lung cancer cells independently. The shRNA and overexpression plasmids of JAK2 were conducted. Results: JAK2 is up-regulated in lung cancer tissues when compared with their adjacent non-tumor tissues, and was associated with lymph node metastasis. Downregulation of JAK2 inhibits the proliferation, migration and invasion abilities of lung cancer cells. Moreover, overexpression of JAK2 induced the proliferation, migration and invasion abilities of lung cancer cells. Conclusion: These findings demonstrate that JAK2, whose expression is up-regulated in lung cancer, may participate in lung cancer progression by regulating cancer cells proliferation, migration and invasion.
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