Browsing by Author "Wei, Shuo"
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Item Nicotinic acid inhibits glioma invasion by facilitating Snail1 degradation(Nature Publishing Group, 2017-03-03) Li, Jiejing; Qu, Jiagui; Shi, Yu; Perfetto, Mark; Ping, Zhuxian; Christian, Laura; Niu, Hua; Mei, Shuting; Zhang, Qin; Yang, Xiangcai; Wei, Shuo; Jiejing Li, Jiagui Qu, Yu Shi, Mark Perfetto, Zhuxian Ping, Laura Christian, Hua Niu, Shuting Mei, Qin Zhang, Xiangcai Yang & Shuo Wei; Wei, ShuoMalignant glioma is a formidable disease that commonly leads to death, mainly due to the invasion of tumor cells into neighboring tissues. Therefore, inhibition of tumor cell invasion may provide an effective therapy for malignant glioma. Here we report that nicotinic acid (NA), an essential vitamin, inhibits glioma cell invasion in vitro and in vivo. Treatment of the U251 glioma cells with NA in vitro results in reduced invasion, which is accompanied by a loss of mesenchymal phenotype and an increase in cell-cell adhesion. At the molecular level, transcription of the adherens junction protein E-cadherin is upregulated, leading to accumulation of E-cadherin protein at the cell-cell boundary. This can be attributed to NA’s ability to facilitate the ubiquitination and degradation of Snail1, a transcription factor that represses E-cadherin expression. Similarly, NA transiently inhibits neural crest migration in Xenopus embryos in a Snail1-dependent manner, indicating that the mechanism of action for NA in cell migration is evolutionarily conserved. We further show that NA injection blocks the infiltration of tumor cells into the adjacent brain tissues and improves animal survival in a rat model of glioma. These results suggest that NA treatment may be developed into a potential therapy for malignant glioma.Item Whole-genome sequencing identifies I-SceI-mediated transgene integration sites in Xenopus tropicalis snai2: eGFP line(G3: Genes | Genomes | Genetics, 2022-02-16) Wang, Jian; Lu, Congyu; Wei, ShuoTransgenesis with the meganuclease I-SceI is a safe and efficient method, but the underlying mechanisms remain unclear due to the lack of information on transgene localization. Using I-SceI, we previously developed a transgenic Xenopus tropicalis line expressing enhanced green fluorescent protein driven by the neural crest-specific snai2 promoter/enhancer, which is a powerful tool for studying neural crest development and craniofacial morphogenesis. Here we carried out whole-genome shotgun sequencing for the snai2: eGFP embryos to identify the transgene integration sites. With a 19x sequencing coverage, we estimated that 6 copies of the transgene were inserted into the X. tropicalis genome in the hemizygous transgenic embryos. Two transgene integration loci adjacent to each other were identified in a non-coding region on Chromosome 1, possibly as a result of duplication after a single transgene insertion. Interestingly, genomic DNA at the boundaries of the transgene integration loci contains short sequences homologous to the I-SceI recognition site, suggesting that the integration was not random but probably mediated by sequence homology. To our knowledge, our work represents the first genome-wide sequencing study on a transgenic organism generated with I-SceI, which is useful for evaluating the potential genetic effects of I-SceI-mediated transgenesis and further understanding the mechanisms underlying this transgenic method.