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The expression of XB130 is associated with invasion and migration of many tumor cells, but its roles in human colorectal cancer (CRC) remains unknown. To investigate this, protein expression levels of XB130 in numerous human CRC cell lines were compared with a normal colorectal mucosa cell line by western blotting. Knockdown of XB130 using small interfering (si)RNA was performed to assess the effects on cell invasion and migration in a Transwell assay and a scratch test. Western blotting was also used to quantify the levels of proteins associated with epithelial‑mesenchymal transition (EMT), including E‑cadherin, vimentin, phosphorylated (p)‑protein kinase B (AKT), p‑forkhead homeobox type O 3a (FOXO3a) and zinc finger E‑box‑binding homeobox 1 (ZEB‑1). The relative expression of XB130 protein was significantly higher in CRC cells compared with control cells (P<0.01). Knockdown of XB130 using siRNA significantly decreased the invasive and migratory responses of CRC cells (P<0.01). In addition, levels of E‑cadherin were increased, while vimentin, p‑AKT, p‑FOXO3a and ZEB‑1 were decreased (P<0.01). In conclusion, the present study demonstrated that the expression of XB130 is elevated in CRC cells. Loss of XB130 was associated with decreased invasion and migration of CRC cells, possibly as a result of EMT inhibition. Thus, upregulation of XB130 may underlie some of the tumorigenic events observed in human CRCs. XB130 may be a promising target for CRC therapy in humans; further mechanistic studies exploring the function of XB130 in CRC cells are warranted.

Objective: To assess the effect as well as mechanism of bone marrow mesenchymal stem cells (BMSCs) modified by the human brain–derived neurotrophic factor gene combined with erythropoietin (EPO) in the treatment of acute spinal cord injury (SCI) in rats. Methods: The Brain-derived neurotrophic factor (BDNF) gene was transected by a virus vector. Rats with SCI were randomly split into following groups: The normal saline (NS) group, the EPO group, The Basso, Beattie, and Bresnahan scores, messenger RNA BDNF expression, and apoptosis rates were compared between the 4 groups at 1, 3, 7, 14, and 21 days after SCI. Results: At 7, 14, and 21 days after operation, the expression of the BDNF gene in the other 3 groups was higher than that of the NS group, and the difference was statistically significant ( P < .05). The apoptosis rate in the combined group was less than that of NS, EPO, and BDNF/BMSC groups, and the differences were statistically significant ( P < .05). Conclusion: Brain-derived neurotrophic factor gene-modified BMSC transplantation combined with EPO can promote the repair of nerve function after SCI in rats.