Emerging roles of lncRNA in cancer and therapeutic opportunities.

Cancer is difficult to cure due to frequent metastasis, and developing effective therapeutic approaches to treat cancer is urgently important. Long non-coding RNAs (lncRNAs) have diverse roles in regulating gene expression at both the transcriptional and translational levels and have been reported to be involved in tumorigenesis and tumor metastasis. In this article, we review the emerging roles of lncRNAs in cancer, especially in cancer immunity, cancer metabolism and cancer metastasis. We also discuss the use of novel technologies, such as antisense oligonucleotides, CRISPR-Cas9 and nanomedicines, to target lncRNAs and thus control cancers.

A new method for calculating the desired laminoplasty opening size based on the target sagittal canal diameter before single-door cervical laminoplasty.

PURPOSE: To build a mathematical model which could calculate the desired laminoplasty opening size (LOS) based on the target sagittal canal diameter (SCD) before single-door cervical laminoplasty (SDCL) when taking the effects of surgery drill into consideration. METHODS: The model was based on geometric analysis on deformation of spinal canal; the formula was derived and characterized as: y (mm) = 2 [Formula: see text] × sin(ß/2) = c - d (y is the size of LOS, [Formula: see text] the size of transverse canal diameter, ß the size of laminoplasty opening size, c the size of mini-plate and d the diameter of the drill bit used during the surgery operation). The parameters of pre- and postoperative computed tomography scans of 20 patients who had undergone SDCL were measured by the picture archiving and communication system (PACS) software and a new instrument named as Lei's ruler, respectively. RESULTS: The effects of surgery SDCL were very significant; for each patient, the SCD was enlarged dramatically after the surgery (P < 0.01). The differences between the data obtained by PACS and Lei's ruler were no statistically significant (P > 0.05). According to the derived formula, the 95% confidence intervals of SCD after the surgery were within the range of 14 mm and 14.5 mm. CONCLUSION: Applying the mathematical model and derived formula, the desired LOS could be calculated according to the target SCD which could help the surgeon select an optimum mini-plate before SDCL. At the same time, a new measuring device named Lei's ruler is designed for the convenience of the derived formula. These slides can be retrieved under Electronic Supplementary Material.

Involvement of IGF-1 receptor signaling pathway in the neuroprotective effects of Icaritin against MPP(+)-induced toxicity in MES23.5 cells.

Icaritin, a natural derivative of Icariin, is the major bioactive component of Epimedium Genus. The present study tested the hypothesis that the neuroprotective effects of Icaritin against 1-Methyl-4-phenylpyridinium ion (MPP(+))-induced toxicity involved activation of the insulin-like growth factor-1 receptor (IGF-1R) signaling pathway in MES23.5 cells. Our results revealed that Icaritin pretreatment attenuated the MPP(+)-induced decrease of cell viability in a dose-dependent fashion. Co-pretreatment with phosphatidylinositol 3-kinase (PI3-K) inhibitor LY294002, mitogen-activated protein kinase (MEK) inhibitor PD98059 or IGF-1 receptor antagonist JB-1 could completely block the protective effects of Icaritin. Moreover, Icaritin pretreatment down-regulated MPP(+)-induced increase of Bax/Bcl-2 ratio transcriptionally and post-transcriptionally. Further study revealed that Icaritin pretreatment could restore the decreased protein expression of Akt and extracellular signal-regulated kinase 1/2 (ERK1/2) induced by MPP(+) and these effects could be completely abolished by LY294002, PD98059 or JB-1. Additionally, Icaritin treatment alone time-dependently enhanced the phosphorylation of Akt and ERK1/2 in MES23.5 cells. The activation of Akt and ERK1/2 by Icaritin could be completely blocked by JB-1, LY294002 or PD98059. Taken together, our data demonstrate that IGF-1 receptor mediated activation of PI3K/Akt and MEK/ERK1/2 signaling pathways are involved in the protective effects of Icaritin against MPP(+)-induced toxicity in MES23.5 cells.