ABSTRACT
There is a pressing need to establish automated solutions for the rapid, high-throughput, and automatic detection of chromosome aberrations (CAs) in the occupational health surveillance of large-scale radiation workers. Here, we described and verified the accuracy of a new measurement system based on the automatic scanning and analysis of dicentric chromosomes (DICs). The effects of cell number on DIC detection by automatic scanning and analysis were studied, and the distribution of DIC values per cell was calculated. In total, 1088 cases were detected by automatic DIC scanning and analysis in 26 663 radiation workers, and 73 cases were further confirmed by a technician, including 5 cases in which radiation exposure lead to harmful medical consequences. Our approach reduces the workload by 96% and increases the speed of assessment approximately 7-fold. Overall, this study validates the utility of a novel rapid and high-throughput CA detection procedure as a means of occupational health surveillance of large-scale radiation workers.
ABSTRACT
BACKGROUND: Proliferation-associated nucleolar protein p120 (NOP2) has been proven to be a promising tumor cell maker, but it has not been specifically studied in colon cancer. This study aims to investigate the role and action mechanism of NOP2 in colon cancer. METHODS: Fluorescence quantitative PCR and western blot assays were used to evaluate the expression of NOP2. NOP2 siRNA was transfected into HCT116, LOVO, and CCK-8 cells, and transwell assays were performed to evaluate the cell proliferation, migration, and invasion. Transcriptome sequencing of both the NOP2 knockdown and negative control (NC) groups was performed. RESULTS: NOP2 expression is significantly upregulated in colon cancer tissues and cells compared with that in the healthy controls. The proliferation, migration, and invasion of the colon cancer cells were significantly suppressed in the NOP2 knockdown group compared with those in the NC group (P<0.05). Transcriptome sequencing showed that ASMTL and C6orf52 were significantly downregulated, while MUC19, TXK, APOBEC2, and RBM44 were upregulated in both of the two NOP2 silenced colon cancer cells relative to those in the control. Gene Ontology (GO) analysis showed that NOP2 knockdown mainly induced differential expression of the genes involved in positive regulation of T cell-mediated cytotoxicity and thiamine metabolism. Kyoto Encyclopedia of Genes and Genomes analysis showed that the gene pathways most significantly affected by NOP2 knockdown were Cytokine-cytokine receptor interaction, Type I diabetes mellitus, Taste transduction, and Systemic lupus erythematosus. CONCLUSIONS: NOP2 promotes proliferation, migration, and invasion of colon cancer cells, and the underlying mechanisms may be related to TXK tyrosine kinase.
ABSTRACT
Tumor-specific hepatic stellate cells (tHSCs) positively participate in human hepatocellular carcinoma (HCC) tumorigenesis and progression. Our previous studies have shown that tHSCs co-culture with dendritic cells (DCs) induced DIgR2 (dendritic cell-derived immunoglobulin receptor 2) expression. The latter is a member of IgSF inhibitory receptor suppressing DCs-initiated antigen-specific T-cell responses. In the current study, we show that hepatic artery injection of DlgR2 siRNA significantly inhibited in-situ HCC xenograft growth in rat livers. Further, 5-FU-medied inhibition of in-situ HCC growth was dramatically sensitized with DlgR2 silence. DlgR2 siRNA injection indeed downregulated DlgR2 in ex-vivo cultured tumor-derived DCs (tDCs). More importantly, tDCs activity was boosted following DlgR2 siRNA. These cells presented with upregulated CD80, CD86 and MHC-II. Production of interleukin-12 and tumor necrosis factor-α was also increased in the DlgR2-silenced tDCs. We propose that DlgR2 knockdown likely boosts the activity of tumor-associated DCs, and inhibits growth of in-situ HCC xenografts.
ABSTRACT
The aim of this study was to explore the effect of apatinib in the treatment of metastatic renal cell carcinoma (mRCC) and related adverse events. A case of mRCC was reported which recurred after surgery and roferon treatment. The patient was treated with apatinib at a dose of 500 mg orally, twice daily, 28 days/cycle. The metastatic lesions improved based on computed tomography after apatinib administration in the fourth and eighth month. The progression-free survival of the patient had increased almost to 8 months. The patient showed a good tolerance with only an adverse effect of mild-to-moderate hand-foot syndrome which was managed well. Apatinib is an option for mRCC after previous treatment. However, more and larger trials are still needed.
