Ockdown promotes tumor cell proliferation, and enhances cellular transformation and tumorigenesis (47), when other groups demonstrated that Dicer knockdown suppresses the growth and tumorigenic capacity of different cancer cell lines (48,49). We demonstrated right here that Dicer knockdown in HCT116 cells impaired cell development and colony formation (Supplementary Figure S9A and B). Surprisingly, Dicer overexpression also repressed cell proliferation and colony formation (Supplementary Figure S9C and D). SIRT7-linked H3K18 deacetylation is crucial for oncogenic transformation, and SIRT7 knockdown impaired the proliferation of HT1080 and U2OS cells (18). Additional investigations are required to address no matter whether the effect of Dicer overexpression on cell development and colony formation will be partially attributed to the reduction of chromatin-associated SIRT7 and therefore hypoacetylation of H3K18Ac. In summary, our study suggest that Dicer overexpression could in part contribute for the growth inhibitory impact of DNA damaging agents, which may perhaps have implication in cancer chemotherapy and radiotherapy. SUPPLEMENTARY Data Supplementary Data are out there at NAR On the web. ACKNOWLEDGEMENT We wish to thank Bin Tan (Chongqing Medical University, Chongqing, China), Xiao Chen, Guiqiang Yang and Yixiang Han (Wenzhou Medical University, Wenzhou, China) for technical assistance, and Quan Wang (Third Military Medical University, Chongqing, China) for supplying MEF cells. FUNDING National Sciences Foundation of China [81171967, 31271383, 81572780 to K.CCL1, Human F.CD44 Protein medchemexpress T.; 31200976 to G.L.]; Na-Nucleic Acids Study, 2016, Vol. 44, No. 8tional Main Special Science and Technologies Project [2013ZX10002002 to K.F.T.]; Zhejiang Provincial National Sciences Foundation [LZ16H160004 to K.PMID:33679749 F.T.]. Funding for open access charge: National Sciences Foundation of China [81171967, 31271383, 81572780 to K.F.T.; 31200976 to G.L.]; National Main Unique Science and Technology Project [2013ZX10002002 to K.F.T.]; Zhejiang Provincial National Sciences Foundation [LZ16H160004 to K.F.T.]. Conflict of interest statement. None declared.18.19. 20.
DOI: 10.15386/cjmed-Original ResearchEFFECT OF CIMETIDINE ON NITRO-OXIDATIVE Stress Within a RAT MODEL OF PERIODONTITISCARINA CULIC1, ALINA ELENA PARVU2, SANDU FLORIN ALB3, CAMELIA ALB4, ANGELA POP1 Division of Odontology, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania two Division of Pathophysiology, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania 3 Division of Periodontology, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania four Division of Propedeutics and Dental Materials, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, RomaniaAbstract Background and aims. Periodontitis is often a chronic inflammation that requires nitro-oxidative tension with damaging periodontal structural effects. We aimed to evaluate the consequences of low-dose cimetidine on nitro-oxidative anxiety in periodontitis. Methods. A rat model of ligature-induced periodontitis was used. Soon after two weeks, the periodontitis groups had been treated with cimetidine, aminoguanidine, N-nitroL-arginine methyl ester and trolox for 1 week. On day 21, blood was drawn plus the serum analyzed for measurement of total nitrites and nitrates, total oxidative status, total antioxidant response, and oxidative pressure index. Benefits. Cimetidine had an inhibitory impact around the synthesis of nitric oxide (p=0.001), total oxidative status (.