Human papillomaviruses (HPVs) including high-risk (HR) and low-risk (LR) subtypes have distinguishable variation on both genotypes and phenotypes. The co-infection of multiple HR-HPVs, headed by HPV16, is common in cervical cancer in female. Recently accumulating reports have focused on the interaction between virus and host, particularly the role of human microRNAs (miRNAs) in anti-viral defense by targeting viral genome. Here, we found a well-conserved target site of miRNAs in the genomes of most HR-HPVs, not LR-HPVs, by scanning all potential target sites of human miRNAs on 24 HPVs of unambiguous subtypes of risk. The site is targeted by two less common human miRNAs, miR-875 and miR-3144, and is located in E6 oncogene open reading frame (ORF) and overlap with the first alternative splice exon of viral early transcripts. In validation tests, miR-875 and miR-3144 were identified to suppress the target reporter activity markedly and inhibit the expression of both synthetically exogenous E6 and endogenous E6 oncogene. High level of two miRNAs can inhibit cell growth and promote apoptosis in HPV16-positive cervical cancer cells. This study provides a promising common target of miRNAs for most HR-HPVs and highlights the effects of two low expressed human miRNAs on tumour suppression.

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Nine phenylethanoid glycosides were isolated from Buddleia lindleyana. On the basis of spectral analyses, their structures were elucidated to be acteoside (1), echinacoside (2), citanoside A (3), leucosceptoside A (4), leucosceptoside B (5), pedicularioside A (6), isoacteoside (7), arenariside (8), and a new compound named buddleoside A (9). The eight known compounds were isolated from this plant for the first time. The neuroprotective effects of compounds 1 (acteoside), 5, 6, 8 and 9 on the 1-methyl-4-phenylpyridinium ion (MPP+)-induced cell death in mesencenphalic neurons were investigated. Mesencenphalic neurons treated with MPP+ underwent cell death as determined by MTT assay. Simultaneous treatment with the phenylethanoid glycosides markedly attenuated MPP+- induced cytotoxicity.

OBJECTIVE To analyze coding SNPs of the HLA-DQA1 gene involved in susceptibility for cervical cancer by a bioinformatics approach, and to choose some SNPs that may have an association with cervical cancer.METHODS By a SNPper tool we extracted SNPs from a public database (dbSNP), exporting them in FASTA formats suitable for subsequent use. Then we used PARSESNP as a tool for the analysis of the cSNPs. RESULTSIn the cSNPs of the HLA-DQA1 gene, we find that rs9272693 and rs9272703, are made up of missense mutations which convert a codon for one amino acid into a codon for a different amino acid. We chose a PSSM Difference >10 as a lower level for the scores of changes predicted to be deldterious. CONCLUSION We used a bioinformatics approach for cSNPs analysis of the HLA-DQA1 gene. This method can select the variants in a conserved region, and give a PSSM Difference score. But the results need to be verified in cervical cancer patients and a control population.