MicroRNA-17 Family Targets RUNX3 to Increase Proliferation and Migration of Hepatocellular Carcinoma.

Hepatocellular carcinoma (HCC) is one common cancer in the world. Previous studies have shown that miR-17 family members are elevated in most tumors and promote tumor progression. However, there is no comprehensive analysis of the expression and functional mechanism of the microRNA-17 (miR-17) family in HCC. The aim of this study is to comprehensively analyze the function of the miR-17 family in HCC and the molecular mechanism of its role. Bioinfoimatics analysis of the miR-17 family expression profile and its relationship to clinical significance using The Cancer Genome Atlas (TCGA) database, and this result was confirmed using quantitative real-time polymerase chain reaction. miR-17 family members were tested for functional effects through transfection of miRNA precursors and inhibitors, and monitoring cell viability and migration by cell count and wound healing assays. In addition, we using dual-luciferase assay and Western blot demonstrated the targeting relationship between the miRNA-17 family and RUNX3. These members of miR-17 family were highly expressed in HCC tissues, and the overexpression of the miR-17 family promoted the proliferation and migration of SMMC-7721 cells, whereas treatment with anti-miR17 inhibitors caused the opposite effects. Notably, we also found that inhibitors anti-each member of miR-17 can suppress the expression of the entire family member. In addition, they can bind to the 3' untranslated region of RUNX3 to regulate its expression at the translational level. Our results proved that miR-17 family has oncogenic characteristics, overexpression every member of the family contributed to HCC cell proliferation and migration by reducing the translation of RUNX3.

Combustion of lean methane over Co3O4 catalysts prepared with different cobalt precursors.

To investigate the effect of catalyst precursors on physicochemical properties and activity of lean methane catalytic combustion, a series of Co3O4 catalysts were prepared via a precipitation method by using four different cobalt precursors: Co(C2H3O2)2, Co(NO3)2, CoCl2, and CoSO4. The catalysts were characterized by BET, XRD, SEM, Raman, XPS, XRF, O2-TPD and H2-TPR techniques. It was found that the different types of cobalt precursor had remarkable effects on the surface area, particle size, reducibility and catalytic performance. In contrast, the Co3O4-Ac catalyst showed a relatively small surface area, but its activity and stability were the highest. XPS, Raman, O2-TPD and H2-TPR results demonstrated that the superior catalytic performance of Co3O4-Ac was associated with its higher Co2+ concentration, more surface active oxygen species and better reducibility. In addition, the activity of the Co3O4-S catalyst reduced significantly due to the residual impurity SO4 2-, which could reduce the concentration of surface adsorbed active oxygen species and inhibit oxygen migration.

The Combination of MoS2/WO3 and Its Adsorption Properties of Methylene Blue at Low Temperatures.

It was found previously that neither monomer MoS2 nor WO3 is an ideal material for the adsorption of organic dyes, while MoS2/WO3 composites synthesized by a two-step hydrothermal method have outstanding adsorption effects. In this work, the chemical state of each element was found to be changed after combination by X-ray photoelectron spectroscopy analysis, which lead to their differences in adsorption performance. Moreover, the adsorption test of methylene blue on MoS2/WO3 composites was carried out under a series of temperatures, showing that the prepared composites also had appreciable adsorption rates at lower temperatures. The adsorption process could be well described by the Freundlich isothermal model and the pseudo-second order model. In addition, the particle-internal diffusion model simulation revealed that the internal diffusion of the particles played an important role in the whole adsorption process.

MicroRNA-497-5p Induces Cell Cycle Arrest Of Cervical Cancer Cells In S Phase By Targeting CBX4.

PURPOSE: miR-497-5p can inhibit cervical cancer cell proliferation. However, the underlying mechanism remains to be elucidated. METHODS: Bioinformatics was used to analyze the target genes of miR-497-5p. qRT-PCR and Western blot were used to analyze mRNA and protein expression, respectively. Dual-luciferase reporter assay was used to analyze the direct binding between miR-497-5p and 3'-untranslated region of CBX4. Cell viability was measured with MTT assay. Flow cytometry was performed to detect cell cycle distribution. RESULTS: Here, using bioinformatics methods we firstly found that miR-497-5p regulated cervical carcinoma proliferation by targeting polycomb chromobox4 (CBX4). Expression of miR-497-5p in cervical carcinoma tissues was negatively correlated with CBX4. A binding region of miR-497-5p in 3'-untranslated region of CBX4 was predicted. Further experiments confirmed that miR-497-5p directly targeted CBX4. Besides, RNA interference of CBX4 inhibited cervical cancer cell proliferation, arrested cells at S phase and reduced the expression of CDK2 and Cyclin A2 proteins. The use of miR-497-5p inhibitor compromised CBX4 interference RNAs induced cycle arrest of cervical cancer cells. Cells co-transfected with miR-497-5p inhibitors and CBX4 interference RNAs had a higher proliferation rate than CBX4 inference RNA-transfected cells. CONCLUSION: All together, the present study demonstrates that miR-497-5p inhibits cervical cancer cells proliferation by directly targeting CBX4.