Objective:To explore the correlation between single nucleotide polymorphisms (SNPs) in Homo sapiens longevity assur-ance homologue 2 (LASS2) gene 3′-untranslated regions (UTR) and susceptibility of bladder cancer among residents of Yunnan, China. Methods:A total of 105 bladder cancer patients (bladder cancer group) and 100 nonbladder cancer patients (control group) were se-lected. PCR method and sequence for LASS2-3′-UTR were performed to identify the SNPs correlated with bladder cancer. The relation-ships between the LASS2-3′-UTR polymorphisms and bladder cancer risk were analyzed. Results:An SNP (rs8444) was identified in LASS2-3′-UTR, and the T/C allele frequencies and genotype distributions of rs8444 largely differed between the bladder cancer and control groups (χ2=10.267, P=0.006;χ2=10.634, P=0.001). Individuals that carry the rs8444 C allele or CC genotype had a remarkably lower risk of bladder cancer compared with those that carry the T allele or TT genotype (OR=0.489, 95%CI:0.309-0.772, P=0.002;OR=0.258, 95%CI:0.081-0.827, P=0.023). No significant correlations were observed between the T/C allele frequencies and genotype distri-butions of rs8444 and TNM stage, as well as histological grade and distant metastasis in bladder cancer (P>0.05). Conclusion: The rs8444 C allele or CC genotype located within LASS2-3′-UTR can lower the susceptibility of bladder cancer among the residents of Yun-nan, China. However, it is not associated with the TNM stage, histological grade, and distant metastasis.

Objective To investigate the main cell types expressed brain-derived neurotrophic factor (BDNF) in the posterior cortical infarction area in cerebral infarction rats after early vein allograft of bone marrow mesenchymal stem cells (BM-MSCs) and the effect of BM-MSCs transplantation on their ce11 numbers and percentages.Methods (1) Fifteen SD rats were randomly divided into sham-operated group 1,ischemia control group 1,and BM-MSCs transplantation group 1 (n=5);distal middle cerebral artery occlusion (dMCA) models were used in the later two groups;1 × 106 CM-DiI labeled BM-MSCs were intravascularly transplanted into the tail vein of rats from the transplantation group 1 at one h after ischemia;all rats were sacrificed 48 h after ischemia;BM-MSCs with co-existence of CM-Dil and BDNF in the ischemia cortex areas were detected by immunofluorescence staining.(2)Fifteen SD rats were randomly divided into sham-operated group 2,ischemia control group 2,and BM-MSCs transplantation group 2 (n=5);dMCAO models were used in the later two groups;1 ×106 non-labeled BM-MSCs were intravascularly transplanted into the tail vein of rats from the transplantation group 2 at one h after ischemia;48 h after ischemia onset,all rats were sacrificed;the number of BDNF+ and CD68+ microglia cells,BDNF+ and Iba-1+ microglia cells,and BDNF+ and neuron-specific nucleoprotein (NeuN)+ neurons were measured by immunofluorescence staining.Results (1) CM-Dil red fluorescence labeled allogeneic BM-MSCs were only found in BM-MSCs transplantation group 1;the labeled cells scattered in the infarct and peri-infarct cortices;9.70％±3.47％ CM-Dil labeled BM-MSCs expressed BDNF,accounting for 13.32％±4.48％ of all BDNF+ cells in the infarct brain cortex.(2) In the brain tissues of cortex infarct area of BM-MSCs transplantation group 2,38.40％±9.04％ BDNF+ cells were Iba-1+ microglia cells,11.65％±2.76％ BDNF+ cells were CD68+ microglia cells,and 28.96％±6.99％ BDNF+ cells were NeuN+ neurons;the Iba-1+ cell numbers and Iba-1+/BDNF+ double positive cell percentages in the BM-MSCs transplantation group 2 ([92.06±36.52]/mm2 and 79.21％±12.27％) were significantly increased as compared with those in the ischemia control group 2 ([31.13±10.23] mm2 and 60.15％±28.20％,P＜0.05).Conclusion Allogeneic BM-MSCs is capable of migrating into the infarct cortex when intravenous transplantation of BM-MSCs is performed at the early stage after ischemia;the main sources of BDNF in these areas are microglias cells and neurons;these BM-MSCs increase both number and percentage of Iba-1+/BDNF+ double positive cells,which may be one of the underlying mechanisms of therapeutic effects.

Objective:To investigate microRNA-20a (miRNA-20a) expression in bladder cancer and its potential mechanism. Methods:MiRNA-20a expression was examined using quantitative reverse-transcription polymerase chain reaction (qRT-PCR) in human bladder cancer tissues and the paired adjacent non-tumor bladder tissues of 96 patients. The target gene of the miRNA-20a was predicted and validated using bioinformatics analysis and reporter gene assay, respectively. The mRNA or protein expression of the target gene in bladder cancer T24 and J82 cells transfected with miRNA-20a mimic or negative control (NC) mimics was detected via qRT-PCR, West-ern blot analysis, and cell immunofluorescence. CCK-8, Transwell chamber, and wound-healing assays were applied to test the prolifer-ation, migration, and invasion of T24 cells after miRNA-20a over-expression in vitro. Results:MiRNA-20a expression significantly in-creased in bladder cancer tissues compared with those in corresponding adjacent non-tumor tissues. High miRNA-20a expression in bladder cancer tissues was closely related to aggressive tumor phenotype, such as high histological grade, poor TNM stage, lymph node invasion, distant metastasis, and tumor recurrence (all P<0.001). Dual-luciferase reporter assay confirmed that miRNA-20a can di-rectly bind to the 3'-untranslated region (3'-UTR) of Homo sapiens longevity assurance homologue 2 (LASS2). Transfection with miRNA-20a mimics significantly inhibited mRNA and protein expression of LASS2 in T24 and J82 cells (all P<0.01) and promoted T24 cell prolif-eration, migration, and invasion in vitro. Conclusion:MiRNA-20a is highly expressed in bladder cancer tissues. MiRNA-20a enhances cell migration as well as proliferation and acts as an oncogene in bladder cancer because of the targeted inhibition of LASS2 expression.