NAD<Superscript>+</Superscript> Treatment Induces Delayed Autophagy in Neuro2a Cells Partially by Increasing Oxidative Stress

NAD⁺ plays important roles in various biological processes. In this study, we reported that treatment of NAD⁺ induces delayed autophagy in Neuro2a cells. Moreover, the effects of NAD⁺ on the autophagy in the cells appear to be, at least partially, mediated by oxidative stress. However, nicotinamide, a degradation product of NAD⁺, does not affect the autophagy. Our experiments have further indicated that the NAD⁺-induced autophagy contributes to the NAD⁺-induced decrease in the survival of these cells. In summary, our study has provided the first evidence that NAD⁺ treatment induces autophagy in cancer cells such as Neuro2a cells, which contributes to the NAD⁺-induced decrease in cancer cell survival.     

IKK�� downregulation is critical for triggering JNKs-dependent cell apoptotic response in the human hepatoma cells under arsenite exposure

Arsenite has a long history in treating leukemia, which might be also effective in the therapy of other cancers. Our previous published data have demonstrated that arsenite exposure induces apoptosis in the HepG2 human hepatoma cells via activating JNKs/AP-1 pathway, but the upstream signaling events responsible for JNKs (c-Jun N-terminal kinase) cascade activation have not been fully discovered. Since cross-talk between IKK/NF-κB and JNKs pathways under stress conditions is a hot topic, in this article, we investigate the potential roles of IKKα and IKKβ, the catalytic subunits of IKK complexes, in the arsenite-induced JNKs pathway activation in the HepG2 cells. We found that arsenite exposure induced JNKs and AP-1 activation accompanying with a significant reduction of both IKKα and IKKβ expressions. Overexpression of IKKβ, but not of IKKα, inhibited arsenite-induced MKK7/JNKs/AP-1 pathway activation as well as the apoptotic response. Therefore, we conclude that the downregulation of IKKβ expression is the prerequisite signaling event for mediating JNKs pathway activation and the cellular apoptotic response in the HepG2 cells under arsenite exposure. Targeting IKKβ might be helpful to enhance the tumor therapeutic effect of arsenite.     

miR-34c inhibits proliferation of glioma by targeting PTP1B

Glioma is one of the most pervasive and invasive primary malignancies in the central nervous sys-tem.Due to its abnormal proliferation,glioma remains hard to cu...     

利用低温水浴鉴定水稻苗期耐寒性

高效准确鉴定苗期耐寒性是水稻(Oryza sativa)耐寒研究的前提。基于流动水浴温度均一这一特性, 建立了一种恒温水浴鉴定水稻幼苗耐寒性方法。该方法中环境温度设定为20°C, 水浴温度设定为4°C。根据对2个水稻亚种不同材料的处理结果, 总结出几种常见品种的低温处理时间与存活率参考值, 并对操作过程中的一些注意事项进行了说明。     

MiR-330-Mediated Regulation of SH3GL2 Expression Enhances Malignant Behaviors of Glioblastoma Stem Cells by Activating ERK and PI3K/AKT Signaling Pathways

MicroRNAs are currently considered as an active and rapidly evolving area for the treatment of tumors. In this study, we elucidated the biological significance of miR-330 in glioblastoma stem cells (GSCs) as well as the possible molecular mechanisms. SH3GL2 is mainly distributed in the central nervous system and considered to be a tumor suppressor in many tumors. In the present study, we identified miR-330 as a potential regulator of SH3GL2 and we found that it was to be inversely correlated with SH3GL2 expression in GSCs which were isolated from U87 cell lines. The expression of miR-330 enhanced cellular proliferation, promoted cell migration and invasion, and dampened cell apoptosis. When the GSCs were co-transfected with the plasmid containing short hairpin RNA directed against human SH3GL2 gene and miR-330 mimic, we found that miR-330 promoted the malignant behavior of GSCs by down-regulating the expression of SH3GL2. Meanwhile, the ERK and PI3K/AKT signaling pathways were significantly activated, leading to the decreased expression of apoptotic protein and increased expression of anti-apoptotic protein. Furthermore, in orthotopic mouse xenografts, the mice given stable over-expressed SH3GL2 cells co-transfected with miR-330 knockdown plasmid had the smallest tumor sizes and longest survival. In conclusion, these results suggested that miR-330 negatively regulated the expression of SH3GL2 in GSCs, which promoted the oncogenic progression of GSCs through activating ERK and PI3K/AKT signaling pathways. The elucidation of these mechanisms will provide potential therapeutic approaches for human glioblastoma.