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We present an insight of the effects of combination therapy with neurotrophin-3 and neural stem cell on functional recovery after spinal cord injury (SCI). Total RNA was extracted from neural stem cell line C17.2 and reversed transcribed into cDNA. Neurotrophin-3 (NT-3) gene was amplified by PCR and subcloned into plasmid to construct an expression vector pNT-3. A positive clone containing pNT-3, named SHN2, was obtained and used for transplantation. Thirty adult mice received mechanical injury at the T8 vertebra level. Cell survival, NT-3 gene expression, and functional recovery were observed through X-Gal staining, RT-PCR, and open field locomotion, respectively. The results show that NT-3 gene comprising 777 bp nucleotides was cloned and a more than twofold expression was detected when transfected into neural stem cell line C17.2. Quantitative analysis of cellular density revealed a significant increase in SHN2 compared to the control cells (p < 0.01). Thirty days after transplantation, SHN2 showed significant increase near the lesion site. Furthermore, the functional recovery indicated an active effect by detecting Basso-Beattie-Bresnahan (BBB) locomotor rating scale (p < 0.01). In conclusion, combined treatment of neural stem cells and NT-3 gene can facilitate functional recovery. It offers an effective approach to treat SCI.

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Abnormal expression of neuropilin and tolloid‐like 1 (NETO1) has been detected in some human carcinomas. However, the expression of NETO1 and the underlying mechanism in epithelial ovarian cancer (EOC) remain unknown. In this study, we found that a higher NETO1 expression in EOC tissue samples compared to normal ovarian tissue samples was significantly correlated with worse overall survival. Additionally, Cox regression analysis suggested that NETO 1 was independently associated with overall survival. NETO1 overexpression enhanced the EOC cells’ migration and invasion capability in vitro via regulation of actin cytoskeleton. Mechanistically, silencing NETO1 reduced the expression of β‐tubulin, F‐actin and KIF2A. In conclusion, our results demonstrated the critical role of NETO1 in EOC invasion, and therapies aimed at inhibiting its expression or activity might significantly control EOC growth, invasion and metastatic dissemination.

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