PubMed · 8111405
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J Worthington, C Pearson, C Julier, J Bell, F B Cornelis. 1993. Dinucleotide repeat polymorphism at the PI locus.. https://doi.org/10.1093/hmg%2F2.12.2203-a
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Although progress in clinical and basic research has significantly increased our understanding of breast cancer, little is known about the molecular mechanism underlying breast cancer metastasis. Identification of effective therapeutic targets to prevent breast cancer metastasis is urgently needed. The function of miR-503-3p has been investigated in other cancers, but its role in breast cancer remains undefined. Here, we found that miR-503-3p was overexpressed in breast cancer tissue and plasma compared with adjacent normal breast tissue and with plasma from healthy individuals. Moreover, we identified miR-503-3p to be an oncogene of breast cancer cell proliferation, migration and invasion. Upregulation of miR-503-3p in breast cancer cells inhibited expression of epithelial-mesenchymal transition (EMT)-related protein SMAD2 and the epithelial marker protein E-cadherin by directly binding to their mRNA 3' untranslated region, whereas increased expression of mesenchymal marker proteins, including vimentin and N-cadherin. Taken together, our findings support a critical role for miR-503-3p in induction of breast cancer EMT and suggest that plasma miR-503-3p may be a useful diagnostic biomarker for breast cancer.
Through exhaustive two-hybrid screens using a budding yeast genomic library, and starting with the splicing factor and DEAH-box RNA helicase Prp22p as bait, we identified yeast Prp45p and Prp46p. We show that as well as interacting in two-hybrid screens, Prp45p and Prp46p interact with each other in vitro. We demonstrate that Prp45p and Prp46p are spliceosome associated throughout the splicing process and both are essential for pre-mRNA splicing. Under nonsplicing conditions they also associate in coprecipitation assays with low levels of the U2, U5, and U6 snRNAs that may indicate their presence in endogenous activated spliceosomes or in a postsplicing snRNP complex.
BACKGROUND: The presence of human papillomavirus (HPV) DNA in relation to cervical cytology was evaluated after treatment of cervical dysplasia. METHODS: Forty patients, 22 with normal and 18 with abnormal cytology (mild or moderate dyskaryosis), with a history of cervical dysplasia were selected. Only patients with HPV DNA positive biopsies obtained before treatment were included. The presence of HPV was assessed in cervical smears at least 1 year after treatment of cervical dysplasia by using a polymerase chain reaction (PCR) with consensus primers (CPI/IIG). HPV typing was done by direct sequence analysis of the CPI/IIG PCR generated amplimers. RESULTS: Smears from 3 of the 22 patients with normal cytology after treatment were positive for HPV DNA (14%). HPV DNA positive smears were found in 13 of the 18 patients with abnormal cytology after treatment (72%) (relative risk: 5.3; 95% confidence interval: 1.78-15.75). In 11 of the 16 HPV DNA positive smears (69%), the HPV type was different from that before treatment. In 35 of 40 patients, the HPV type before treatment could not be detected after treatment (88%). CONCLUSIONS: A minority of the patients with normal cytology after treatment of cervical dysplasia had detectable HPV DNA. In contrast, a high prevalence of HPV DNA was found in cervical smears of patients with abnormal cytology after treatment of cervical dysplasia. After treatment, none of the patients with abnormal cytology but HPV DNA negative smears had recurrence of cervical intraepithelial neoplasia. This suggests the value of supplementary HPV DNA testing during follow-up of patients treated for cervical dysplasia.