Long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) promote cell proliferation in colorectal cancer by affecting P53.

OBJECTIVE: Colorectal cancer (CRC) is one of the most frequent malignant tumors worldwide. The connection between lncRNAs expression and CRC development has not been well identified in the recent literature. This study focuses on the role of lncRNA-SNHG1 on CRC progression and development. The quantitative Real-time PCR (qRT-PCR) assay was conducted to identify the expression level of small nucleolar RNA host gene 1 (SNHG1). PATIENTS AND METHODS: Cell proliferation and viability were examined by 3-(4,5)-dimethylthiazol(-z-y1)-3,5-diphenyl tetrazoliumbromide (MTT assay) and colony formation assay. Cell apoptosis and cell cycle distribution were detected by flow cytometry. RESULTS: Expressions of p53, p21, BAX were assessed by Western blotting. CRC cells transfected with lncRNA-shRNA were injected into nude mice to identify the role of SNHG1 on tumorigenesis in vivo. SNHG1 expression level was elevated in CRC tissues when compared to adjacent tissues (n=86). SNHG1 knockdown significantly suppressed cell proliferation and viability, while SNHG1 overexpression had the opposite effect. Decreased SNHG1 expression enhanced cell apoptosis and triggered cell cycle arrest in G0/G1 phase, while elevated SNHG1 expression done the opposite. Besides, downregulation of SNHG1 impeded tumorigenesis in vivo. Protein levels of p53 and p53 target genes were affected by SNHG1 in vitro. CONCLUSIONS: Our research demonstrated that SNHG1 may participate in controlling CRC proliferation, viability, and apoptosis via modulating p53 partially, which provides potential therapeutic targets for CRC.

Ethyl carbamate levels in wine and spirits from markets in Hebei Province, China.

Ethyl carbamate (EC) in wine, grain spirits and wine sauce (145 samples) was analysed using solid-phase extraction and stable isotope dilution GC/MS. Samples were obtained from markets in eight areas (Shijiazhuang, Baoding, Handan, Qinhuangdao, Langfang, Zhangjiakou, Xingtai and Cangzhou) of Hebei Province, China. The method had a limit of detection of 2 µg kg⁻¹, with recoveries varying from 95.7 to 102% and RSD ranging 2.3-5.6%. The average concentrations of ethyl carbamate in wines, grain spirits and wine sauce were 14.7 (<2.0-44.5) µg kg⁻¹, 33.8 (2.9-129) µg kg⁻¹ and 8.7 (<2.0-63.3) µg kg⁻¹, respectively. The results led to the development of limit standards that can be used to predict the concentration of ethyl carbamate in Chinese fermented wines.

Analysis of RUNX1 binding site and RAPTOR polymorphisms in psoriasis: no evidence for association despite adequate power and evidence for linkage.

BACKGROUND: A previous study identified two peaks of allelic association between psoriasis and single nucleotide polymorphisms (SNPs) mapping to distal chromosome 17q, including a disease associated SNP that leads to loss of a RUNX1 transcription factor binding site, and additional SNPs in the third intron of the RAPTOR gene. Another study found an association with SNPs in the RAPTOR gene, but not with the RUNX1 binding site polymorphism. METHODS: In an effort to confirm these observations, we genotyped 579 pedigrees containing 1285 affected individuals for three SNPs immediately flanking and including the RUNX1 binding site, and for three SNPs in the RAPTOR gene. RESULTS: Here we report further evidence for linkage to distal chromosome 17q, with a linkage peak mapping 1.7 cM distal to the RUNX1 binding site (logarithm of the odds 2.26 to 2.73, depending upon statistic used). However, we found no evidence for association to individual SNPs or haplotypes in either of the previously identified peaks of association. Power analysis demonstrated 80% power to detect significant association at genotype relative risks of 1.2 (additive and multiplicative models) to 1.5 (dominant and recessive models) for the RUNX1 binding site, and 1.3 to 1.4 for the RAPTOR locus under all models except dominant. CONCLUSIONS: Our data provide no support for the previously identified RUNX1 binding site or for the RAPTOR locus as genetic determinants of psoriasis, despite evidence for linkage of psoriasis to distal chromosome 17q.