276 research outputs found
PReS-FINAL-2108: Long-term outcome of 114 adult JIA patients in a non-pediatric rheumatology institute in Japan
20th Congress of Paediatric Rheumatology European Society 2013年09月25日 Sloveni
PReS-FINAL-2108: Long-term outcome of 114 adult JIA patients in a non-pediatric rheumatology institute in Japan
20th Congress of Paediatric Rheumatology European Society 2013年09月25日 Sloveni
Prevalence of polymorphisms of the genes responsible for auto-inflammatory diseases among 236 patients with recurrent fever in a rheumatology institute in Japan
POSTER PRESENTAION8th International Congress of Familial Mediterranean Fever and Systemic Autoinflammatory Diseases/30 September - 3 October 2015/Dresden, German
Overexpression of SMYD2 in gastric cancer
Background: SET and MYND domain-containing protein 2 (SMYD2) is a lysine methyltransferase for histone H3, p53 and Rb and inhibits their transactivation activities. In this study, we tested whether SMYD2 (1q42) acts as a cancer-promoting factor by being overexpressed in gastric cancer.
Methods: We analysed 7 gastric cancer cell lines and 147 primary tumor samples of gastric cancer, which were curatively resected in our hospital.
Results: SET and MYND domain-containing protein 2 was detected in these cell lines (five out of seven cell lines; 71.4%) and primary tumor samples (fifty-six out of one hundred and forty-seven cases; 38.1%). Knockdown of SMYD2 using specific small interfering RNA inhibited proliferation, migration and invasion of SMYD2-overexpressing cells in a TP53 mutation-independent manner. Overexpression of SMYD2 protein correlated with larger tumor size, more aggressive lymphatic invasion, deeper tumor invasion and higher rates of lymph node metastasis and recurrence. Patients with SMYD2-overexpressing tumours had a worse overall rate of survival than those with non-expressing tumours (P=0.0073, log-rank test) in an intensity and proportion score-dependent manner. Moreover, multivariate analysis demonstrated that SMYD2 was independently associated with worse outcome (P=0.0021, hazard ratio 4.25 (1.69–10.7)).
Conclusions: These findings suggest that SMYD2 has a crucial role in tumor cell proliferation by its overexpression and highlight its usefulness as a prognostic factor and potential therapeutic target in gastric cancer
PReS-FINAL-2125: A Japanese girl with childhood-onset anti-Ku antibody positive generalized morphea-myositis overlap syndrome
POSTER PRESENTATIONProceedings of 20th Pediatric Rheumatology European Society (PReS) Congress / 25-29 September 2013 / Ljubljana, Sloveni
The Escherichia coli SOS Gene dinF Protects against Oxidative Stress and Bile Salts
DNA is constantly damaged by physical and chemical factors, including reactive oxygen species (ROS), such as superoxide radical (O2−), hydrogen peroxide (H2O2) and hydroxyl radical (•OH). Specific mechanisms to protect and repair DNA lesions produced by ROS have been developed in living beings. In Escherichia coli the SOS system, an inducible response activated to rescue cells from severe DNA damage, is a network that regulates the expression of more than 40 genes in response to this damage, many of them playing important roles in DNA damage tolerance mechanisms. Although the function of most of these genes has been elucidated, the activity of some others, such as dinF, remains unknown. The DinF deduced polypeptide sequence shows a high homology with membrane proteins of the multidrug and toxic compound extrusion (MATE) family. We describe here that expression of dinF protects against bile salts, probably by decreasing the effects of ROS, which is consistent with the observed decrease in H2O2-killing and protein carbonylation. These results, together with its ability to decrease the level of intracellular ROS, suggests that DinF can detoxify, either direct or indirectly, oxidizing molecules that can damage DNA and proteins from both the bacterial metabolism and the environment. Although the exact mechanism of DinF activity remains to be identified, we describe for the first time a role for dinF
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