NCK1-AS1 enhances glioma cell proliferation, radioresistance and chemoresistance via miR-22-3p/IGF1R ceRNA pathway.

Glioma is the deadliest disease in human central nerve system. Abnormal expression of long noncoding RNA (lncRNA) expression has been demontrated to be implicated in various cancers. The oncogenic role of lncRNA NCK1-AS1 has been validated in cervical cancer, wheras its role in glioma remians obscure. Our research findings suggested that NCK1-AS1 was upregulated in glioma tissues and cells. NCK1-AS1 deficiency hindered cell proliferation and enhanced cell apoptosis. Additionally, the chemoresistance and radioresistance of glioma cells were impaired by NCK1-AS1 depletion. Moreover, miR-22-3p, a downstream gene of NCK1-AS1, could weaken glioma cell chemoresistance and radioresistance. Similarly, IGF1R was the downstream target gene of miR-22-3p. Further mechanism and function assays demonstrated that NCK1-AS1 promoted glioma cell growth, chemoresistance and radioresistance via sponging miR-22-3p to upregulate IGF1R. Finally, the tumor facilitator function of NCK1-AS1 was also verified by in vivo experiments. Taken together, NCK1-AS1 contributes to glioma cell proliferation, radioresistance and chemoresistance via miR-22-3p/IGF1R ceRNA pathway, which might provide a new insight for improving the radiotherapy and chemotherapy treatments of glioma.

lncRNA CCAT1 Promotes Glioma Tumorigenesis by Sponging miR-181b.

Colon cancer-associated transcript 1 (CCAT1), a long non-coding RNA (lncRNA), is upregulated and has a vital role in the pathogenesis of numerous cancers. Recently, its high expression was found in glioma tissues. miR-181b is downregulated in glioma and acts as a tumor suppressor. However, the exact mechanism of CCAT1 action in the regulation of glioma development remains unknown. CCAT1 and miR-181b expression was firstly examined in glioma tissue samples by real-time PCR. An RNA interference approach was used to downregulate CCAT1 expression and we analyzed the underlying mechanism of CCAT1 by using bioinformatics analysis, CCK-8 assay, Transwell assay, flow cytometry, luciferase assay, RNA immunoprecipitation, real-time PCR, Western blot, and xenograft models. CCAT1 expression was significantly increased, while miR-181b decreased, in glioma tissues. Interestingly, miR-181b expression was negatively correlated with the CCAT1 level in glioma samples. Knockdown of CCAT1 notably suppressed proliferation, migration and the epithelial-mesenchymal transition (EMT) process, and promoted the apoptosis of U87 and LN229 glioma cells, which could be enhanced by transfection with miR-181b mimic while it was abolished by anti-miR-181b. Additionally, we found that CCAT1 may act as a competing endogenous RNA (ceRNA) for miR-181b, regulating the de-repression of FGFR3 and PDGFRα. In conclusion, CCAT1 promotes glioma tumorigenesis by sponging miR-181b, leading to the de-repression of its endogenous targets FGFR3 and PDGFRα, which provides a potential therapeutic target for glioma treatment. J. Cell. Biochem. 118: 4548-4557, 2017. © 2017 Wiley Periodicals, Inc.

Protection of ginsenoside Rg1 on central nerve cell damage and the influence on neuron apoptosis.

This paper aimed to verify the function of ginsenoside in the repair of peripheral nerve injury through the model of sciatic nerve injury in rat. The method was to prepare the model of SD rat injury of sciatic nerve, and to conduct treatment with different dose of ginsenoside Rg1. At the same time, the control group was established. The regenerative repair, functional recovery and the situation of target organ, etc. were evaluated by neuromorphic metrology index, fluorescence gold retrograde tag, animal behavior index (sciatic nerve index). The result was the situation of nerve regenerative repair and functional recovery in high dose ginsenoside Rg1 group was obviously superior to other groups, the recovery of sciatic nerve index, target muscle, etc. were fine and mostly close to normal. It was concluded that ginsenoside Rg1 could effectively promote the regenerative repair of peripheral nerve injury, and accelerate the recovery of its nerve function. It could also promote the regeneration of peripheral nerve and the recovery of its nerve function.

Human umbilical cord blood-derived mesenchymal stem cell transplantation for the treatment of spinal cord injury.

The aim of the present study was to investigate the effects of human umbilical cord blood-derived mesenchymal stem cell (HUCB-MSC) transplantation on the functional restoration of spinal cord injury (SCI). A total of 46 adult Wistar rats were randomly divided into three groups: Injury (n=15), control (n=15) and transplantation (n=16). A SCI model was established using the modified Allen's method (vulnerating energy, 25 g/cm). The rats in the control and transplantation groups were injected at the site of the injury with physiological saline and HUCB-MSC suspension, respectively. At week one, two and four following treatment, the behavior of the rats was evaluated using the Basso, Beattie, Bresnahan locomotor rating scale. In addition, immunohistochemistry (IHC) was performed on samples from the rats that had been sacrificed four weeks subsequent to the treatment. Recovery of the spinal cord nerve function was identified to be significantly different at week two and four following treatment (P<0.05), and IHC identified that at week four following treatment novel nerve cells were being produced. Thus, transplantation of HUCB-MSCs promoted the recovery of the damaged function of spinal cord nerves in rats with SCI.