Construction of Core–Shell NiMoO₄@Ni-Co‑S Nanorods as Advanced Electrodes for High-Performance Asymmetric Supercapacitors

In this work, hierarchical core–shell NiMoO₄@Ni-Co-S nanorods were first successfully grown on nickel foam by a facile two-step method to fabricate a bind-free electrode. The well-aligned electrode wrapped by Ni-Co-S nanosheets displays excellent nanostructural properties and outstanding electrochemical performance, owing to the synergistic effects of both nickel molybdenum oxides and nickel cobalt sulfides. The prepared core–shell nanorods in a three-electrode cell yielded a high specific capacitance of 2.27 F cm^–2 (1892 F g^–1) at a current density of 5 mA cm^–2 and retained 91.7% of the specific capacitance even after 6000 cycles. Their electrochemical performance was further investigated for their use as positive electrode for asymmetric supercapacitors. Notably, the energy density of the asymmetric supercapacitor device reached 2.45 mWh cm^–3 at a power density of 0.131 W cm^–3, and still retained a remarkable 80.3% of the specific capacitance after 3500 cycles. There is great potential for the electrode composed of the core–shell NiMoO₄@Ni-Co-S nanorods for use in an all-solid-state asymmetric supercapacitor device

<i>HOXB1</i> Is a Tumor Suppressor Gene Regulated by miR-3175 in Glioma

<div><p>The <i>HOXB1</i> gene plays a critical role as an oncogene in diverse tumors. However, the functional role of HOXB1 and the mechanism regulating HOXB1 expression in glioma are not fully understood. A preliminary bioinformatics analysis showed that HOXB1 is ectopically expressed in glioma, and that HOXB1 is a possible target of miR-3175. In this study, we investigated the function of HOXB1 and the relationship between HOXB1 and miR-3175 in glioma. We show that HOXB1 expression is significantly downregulated in glioma tissues and cell lines, and that its expression may be closely associated with the degree of malignancy. Reduced HOXB1 expression promoted the proliferation and invasion of glioma cells, and inhibited their apoptosis in vitro, and the downregulation of HOXB1 was also associated with worse survival in glioma patients. More importantly, HOXB1 was shown experimentally to be a direct target of miR-3175 in this study. The downregulated expression of miR-3175 inhibited cell proliferation and invasion, and promoted apoptosis in glioma. The oncogenicity induced by low HOXB1 expression was prevented by an miR-3175 inhibitor in glioma cells. Our results suggest that HOXB1 functions as a tumor suppressor, regulated by miR-3175 in glioma. These results clarify the pathogenesis of glioma and offer a potential target for its treatment.</p></div

HOXB1 is a direct target of miR-3175.

<p><b>(A)</b> Diagram of the seed sequence of the miR-3175-binding site within the wild-type HOXB1 3′-UTR and the design of the mutated HOXB1 3′-UTR sequence. The mutated HOXB1 3′-UTR sequence is labeled in red. <b>(B)</b> Luciferase assay of U87 cells after cotransfection with the wild-type or mutant HOXB1 3′-UTR and miR-3175 mimics or miR-3175 mimics NC. The pRL-TK Renilla luciferase reporter vector was used as the internal control. Luciferase activity = firefly luciferase/Renilla luciferase. <b>(C)</b> HOXB1 mRNA expression is modulated by miR-3175. Glioma cell lines were transfected with miR-3175 mimics, miR-3175 inhibitor and the corresponding NCs, and incubated for 72 h. Cells were harvested and assayed using qRT-PCR. <b>(D-E)</b> Western blot analysis of HOXB1 protein levels in glioma cell lines after transfection with miR-3175 mimics, miR-3175 inhibitor and the corresponding NCs at 72 h. <b>(F)</b> The correlation between HOXB1 and miR-3175 expression in human glioma tissue specimens was analyzed with Spearman’s rank correlation. All results are representative of three independent experiments, and a statistical analysis is performed (mean ± SD, *<i>P</i> < 0.05, **<i>P</i> < 0.01, and ***<i>P</i> < 0.001).</p

Aberrant expression of miR-3175 in glioma cell lines affects their proliferation, invasion, and apoptosis.

<p><b>(A)</b> MiR-3175 expression levels in 40 human glioma tissue specimens and 8 non-neoplastic brain tissue specimens were assessed by qRT-PCR. <b>(B)</b> qRT-PCR analysis showed miR-3175 expression in glioma cell lines A172, U251, and U87. <b>(C)</b> Equal concentrations of miR-3175 mimics, mimics NC, miR-3175 inhibitor and inhibitor NC were transfected into U87 cells using Lipofectamine 2000. The expression levels of miR-3175 were evaluated by qRT-PCR at 24 h after transfection. <b>(D)</b> An MTT cell proliferation assay was performed at 48 h after transfection with equal concentrations of miR-3175 inhibitor and inhibitor NC in glioma cell lines. <b>(E-F)</b> Scratch wound assay of glioma cell lines transfected with equal concentrations of miR-3175 inhibitor and inhibitor NC. The wound gaps were photographed and measured at 0 and 24 h (40 ×, Scale bars = 200 μm). <b>(G-H)</b> Transwell assay of glioma cell lines transfected with equal concentrations of miR-3175 inhibitor and inhibitor NC. The migrated cells were photographed and counted in three non-overlapping, randomly selected fields (100 ×, Scale bars = 200 μm). <b>(I-J)</b> Flow cytometric analysis of apoptosis in glioma cell lines after transfection with equal concentrations of miR-3175 inhibitor and inhibitor NC. Apoptosis was assessed with Annexin V-FITC/PI. All results are representative of three independent experiments, and a statistical analysis is performed (mean ± SD, *<i>P</i> < 0.05, **<i>P</i> < 0.01, and ***<i>P</i> < 0.001).</p

Oncogenicity induced by low HOXB1 expression is prevented by miR-3175 inhibitor in glioma cells.

<p><b>(A)</b> An MTT cell proliferation assay was performed at 48 h after transfection with si-NC + inhibitor NC, si-HOXB1 + miR-3175 inhibitor and si-HOXB1 + inhibitor NC in glioma cell lines. <b>(B-C)</b> Flow cytometric analysis of apoptosis in glioma cell lines after transfection with si-NC + inhibitor NC, si-HOXB1 + miR-3175 inhibitor and si-HOXB1 + inhibitor NC. Apoptosis was assessed with Annexin V-FITC/PI. <b>(D-E)</b> Western blot analysis of several apoptosis-related proteins (procaspase-3, p53 and cytochrome c) expression in U87 cells after transfection with si-NC + inhibitor NC, si-HOXB1 + miR-3175 inhibitor and si-HOXB1 + inhibitor NC. All results are representative of three independent experiments, and a statistical analysis is performed (mean ± SD, *<i>P</i> < 0.05, **<i>P</i> < 0.01, and ***<i>P</i> < 0.001).</p

The role of HOXB1 in glioma cell proliferation, invasion, and apoptosis.

<p><b>(A-C)</b> Three siRNA targeting different sites of HOXB1 and a siRNA negative control (si-NC) were transfected into U87 cells using Lipofectamine 2000. Total mRNA or total protein was isolated at 24 h or 48 h after transfection. HOXB1 mRNA expression was assessed by qRT-PCR. HOXB1 protein expression was determined with western blot analysis. si-HOXB1-2 as the most efficient siRNA was used in further studies. <b>(D)</b> An MTT cell proliferation assay was performed at 48 h after transfection with equal concentrations of si-HOXB1 and si-NC in glioma cell lines. <b>(E-F)</b> Scratch wound assay of glioma cell lines transfected with equal concentrations of si-HOXB1 and si-NC. A linear wound was made with a 200 μl pipette tip and the wound width was recorded at three different reference points after 0 and 24 h (40 ×, Scale bars = 200 μm). <b>(G-H)</b> Transwell assay of glioma cell lines transfected with equal concentrations of si-HOXB1 and si-NC. The migrated cells were fixed with 4% paraformaldehyde, stained with Giemsa and calculated with microscope in three non-overlapping, randomly selected fields (100 ×, Scale bars = 200 μm). <b>(I-J)</b> Flow cytometric analysis of apoptosis in glioma cell lines after transfection with equal concentrations of si-HOXB1 and si-NC. Apoptosis was assessed with Annexin V-FITC/PI. All results are representative of three independent experiments, and a statistical analysis is performed (mean ± SD, *<i>P</i> < 0.05, **<i>P</i> < 0.01, and ***<i>P</i> < 0.001).</p

Multivariate Cox regression analysis of prognostic factors in glioma patients.

<p>^<b>a</b> Data from imaging measurement.</p><p>^<b>b</b> Patients who suffer from enormous tumor both in frontal lobe, parietal lobe and temporal lobe are counted repeatedly.</p><p>Multivariate Cox regression analysis of prognostic factors in glioma patients.</p