Existence of independent C/EBPβ 3＇-UTR RNA in human tissues

Two years ago, it was found that the RNA expressed from the promoter in the 3＇-untranslated region （UTR） of a gene, i.e. independent 3＇-UTR RNA, exists widely in human, mouse, and fly [1].     

Histone acetyltransferase p300 regulates the expression of human pituitary rumor transforming gene （hPTTG）

The human pituitary tumor transforming gene （hPTTG） serves as a marker for malignancy grading in several cancers, hPTTG is involved in multiple cellular pathways including cell transformation, apoptosis, DNA repair, genomic instability, mitotic control and angiogenesis induction. However, the molecular mechanisms underlying hPTTG regulation have not been fully explored. In this study, we found that overexpression of histone acetyltransferase （HAT） p300 upregulated hPTTG at the levels of promoter activity, mRNA and protein expression. Moreover, the HAT activity of p300 was critical for its regulatory function. Chromatin immunoprecipitation （CHIP） analysis revealed that overexpression of p300 elevated the level of histone H3 acetylation on the hPTTG promoter. Additionally, the NF-Y sites at the hPTTG promoter exhibited a synergistic effect on upregulation of hPTTG through interacting with p300. We also found that treatment of 293T cells with the histone deacetylase （HDAC） inhibitor Tfichostatin A （TSA） increased hPTTG promoter activity. Meanwhile, we provided evidence that HDAC3 decreased hPTTG promoter activity. These data implicate an important role of the histone acetylafion modification in the regulation of hPTTG.     

Different Effects of Homocysteine and Oxidized Low Density Lipoprotein on Methylation Status in the Promoter Region of the Estrogen Receptor α Gene

We investigated the effects of homocysteine (Hcy) and oxidized low density lipoprotein (ox-LDL) on DNA methylation in the promoter region of the estrogen receptor α (ERos) gene,and its potentialmechanism in the pathogenesis of atherosclerosis.Cultured smooth muscle cells (SMCs) of humans weretreated by Hcy and ox-LDL with different concentrations for different periods of time.The DNA methylationstatus was assayed by nested methylation-specific polymerase chain reaction,the lipids that accumulated inthe SMCs and foam cell formations were examined with Oil red O staining.The proliferation of SMCs wasassayed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide method.The results showedthat ox-LDL in moderate concentrations (10-40 mg/L) induced de novo methylation in the promoter regionof the ERα gene of SMCs.However,high concentrations (50 mg/L) of ox-LDL,resulted in demethylation ofERα.The Hcy treatment resulted in de novo methylation in the promoter region of the ERα gene with aconcentration- and treating time-dependent manner,and a dose-dependent promoting effect on SMCproliferation.These data indicated that the two risk factors for atherosclerosis had the function of inducingde novo methylation in the promoter region of the ERα gene of SMCs. However,high concentrations (50rag/L) of ox-LDL induced demethylation,indicating that different risk factors of atherosclerosis with differentpotency might cause different aberrant methylation patterns in the promoter region of the ERα gene.Theatherogenic mechanism of Hcy might involve the hypermethylation of the ERα gene,leading to the proliferationof SMCs in atherosclerotic lesions.