Ectopic glucose-6-phosphate dehydrogenase (G6PD) expression may contribute to tumorigenesis in cervical cancer associated with high-risk human papillomavirus (HR-HPV 16 and 18) infections. Here, we demonstrate that microRNA-1 (miR-1) in association with AGO proteins targets G6PD in HR-HPV-infected human cervical cancer cells. miR-1 inhibited expression of a reporter construct containing a putative G6PD 3′-UTR seed region and suppressed endogenous G6PD expression. Down-regulation of miR-1 increased G6PD expression in cervical cancer cells. Regression analysis revealed that miR-1 levels correlate negatively with the clinicopathologic features in HR-HPV 16/18-infected cervical cancer patients. miR-1 overexpression inhibited proliferation and promoted apoptosis in cervical cancer cells and reduced xenograft tumor growth in nude mice. Conversely, sponge-mediated miR-1 knockdown markedly increased viability and reduced apoptosis in cervical cancer cells and supported neoplasm growth. Restoration of G6PD expression partially reversed the effects of miR-1 overexpression both in vitro and in vivo. In addition, co-transfection of G6PD siRNA and miR-1 sponge partially reversed miR-1 sponge-induced reductions in cell viability and neoplasm growth. These results suggest that miR-1 suppresses the development and progression of HR-HPV 16/18-infected cervical cancer by targeting G6PD and may be a promising novel therapeutic candidate.

Voltage-gated sodium channels beta 2 (Navβ2, encoded by SCN2B) is a substrate of β-site amyloid precursor protein cleaving enzyme 1 (BACE1) and regulates cell surface expression of channels in neurons. Previous studies reported enhanced Navβ2 processing by BACE1 in Alzheimer’s disease (AD) model and patients. We investigated whether changes in Navβ2 expression affect neuronal seizure and amyloid precursor protein (APP) processing in an AD mouse model. Our study used eight-month-old APP/presenilin 1 (PS1) mice and transgenic Navβ2 knockdown [by 61% vs. wild type (WT)] APP/PS1 mice (APP/PS1/Navβ2-kd), with age-matched WT and Navβ2 knockdown (Navβ2-kd) mice as controls. We found that Navβ2 knockdown in APP/PS1 mice partially reversed the abnormal Navβ2 cleavage and the changes in intracellular and total Nav1.1α expression. It also restored sodium currents density in hippocampal neurons and neuronal activity, as indicated by EEG tracing; improved Morris water maze performance; and shifted APP amyloidogenic metabolism towards non-amyloidogenic processing. There were no differences in these indicators between WT and Navβ2-kd mice. These results suggest Navβ2 knockdown may be a promising strategy for treating AD.

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With the development of communications industry, mobile phone plays an important role in daily life. Whether or not the electromagnetic radiation emitted by mobile phone causes any adverse effects on brain function has become of a great concern. This paper investigated the effect of electromagnetic field on spatial learning and memory in rats. 32 trained Wistar rats were divided into two groups: exposure group and control group. The exposure group was exposed to 916 MHz, 10w/m2 mobile phone electromagnetic field (EMF) 6 h a day, 5 days a week, 10 weeks. The completion time, number of total errors and the neuron discharge signals were recorded while the rats were searching for food in an eight-arm radial maze at every weekend. The neuron signals of one exposed rat and one control rat in the maze were obtained by the implanted microelectrode arrays in their hippocampal regions. It can be seen that during the weeks 4-5 of the experiment, the average completion time and error rate of the exposure group were longer and larger than that of control group (p < 0.05). During the weeks 1-3 and 6-9, they were close to each other. The hippocampal neurons showed irregular firing patterns and more spikes with shorter interspike interval during the whole experiment period. It indicates that the 916 MHz EMF influence learning and memory in rats to some extent in a period during exposure, and the rats can adapt to long-term EMF exposure.

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