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In this research, the adsorptive removal of diclofenac sodium, one of the representative pharmaceuticals and personal care products, from aqueous solution using FeO@MOF-100(Fe) magnetic microspheres was studied for the first time. The FeO@MOF-100(Fe) microspheres exhibit strong magnetism and stability, which were observed as a core-shell structure. The maximum adsorption capacity of FeO@MOF-100(Fe) for diclofenac sodium can reach 377.36 mg L, which was higher than most of the adsorbents reported. The adsorption kinetics follows the pseudo-second-order kinetic equation. And the adsorption equilibrium of DCF can be described with Langmuir isotherm. In the cycle experiment, FeO@MOF-100(Fe) material performed high adsorption efficiency for low-concentration diclofenac sodium solution, and the removal rate can still reach 80% after 5 cycles of adsorption without desorption. The mechanisms including electrostatic interaction, H-bond interaction, and π-π interaction that coexisted in the adsorption processes would be of benefit to enhance the adsorption capacity. The FeO@MOF-100(Fe) magnetic microspheres offer exciting opportunities for further application.

Metastasis is the primary cause of death in lung cancer patients and EMT (epithelial-mesenchymal transition) promotes metastasis. Previous study revealed that DAL-1 (differentially expressed in adenocarcinoma of the lung) could attenuate EMT and metastasis in non-small cell lung cancer (NSCLC). Further study proved that HSPA5 (heat shock protein 5), which has a promoting effect on EMT, could bind to DAL-1. In this study, the mRNA and protein expression levels of target molecules were detected by RTq-PCR and western blot assays, the migration and invasion abilities were examined by Transwell migration and invasion assay, and the proliferation ability was measured by CCK-8 assay. We revealed that DAL-1 was downregulated while HSPA5 was upregulated in NSCLC and found the protein of DAL-1 and HSPA5 co-localized in the cytoplasm and nucleus. We demonstrated that DAL-1 can suppress the expression of HSPA5 on mRNA and protein levels, and decrease EMT, migration, invasion and proliferation abilities by down-regulating HSPA5. Furthermore, we discovered that DAL-1 plays a role in inhibiting PI3K/Akt/Mdm2 signaling pathway by suppressing HSPA5.

Lung cancer is the leading cause of cancer-related death worldwide. The poor prognosis is partly due to lack of efficient methods for early diagnosis. MicroRNAs play roles in almost all aspects of cancer biology, and can be secreted into the circulation and serve as molecular biomarkers for the early diagnosis of cancer. In the present study, we determined the expression of miR-96 and the function of its target genes in lung cancer through bioinformatic analysis. Four microRNA expression profiles of lung cancer were downloaded from Gene Expression Omnibus and the data were analyzed using SPSS 16.0 software. Compared to the control group, expression of miR-96 was significantly increased in non-small cell lung cancer (NSCLC) (GSE51855), lung adenocarcinoma (GSE48414), stage I adenocarcinoma tissues (GSE63805) and the plasma of lung cancer patients (GSE68951). miR-96 was also elevated in six different NSCLC cell lines. However, the expression level of miR-96 was not related to the age, gender, clinical stage and histological subtype of the NSCLC patients. GO analysis of 78 predicted target genes of miR-96 showed that 42 of the obtained GO terms are highly associated with specific cellular processes including response to stimulus, signaling pathway, cell division, cell communication, cell migration and calcium signaling. KEGG results indicated that the miR-96 targets are mainly involved in the GnRH signaling pathway, long-term potentiation and insulin signaling pathway. In conclusion, miR-96, functioning as an oncogene, may play an important role in the development and progression of lung cancer. miR-96 may have the potential to serve as a molecular biomarker for the early diagnosis of NSCLC.