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Objective. We investigated the expression levels of both FOSL2 mRNA and protein as well as evaluating DNA methylation in the blood of type 2 diabetes mellitus (T2DM) Uyghur patients from Xinjiang. This study also evaluated whether FOSL2 gene expression had demonstrated any associations with clinical and biochemical indicators of T2DM. Methods. One hundred Uyghur subjects where divided into two groups, T2DM and nonimpaired glucose tolerance (NGT) groups. DNA methylation of FOSL2 was also analyzed by MassARRAY Spectrometry and methylation data of individual units were generated by the EpiTyper v1.0.5 software. The expression levels of FOS-like antigen 2 (FOSL2) and the protein expression levels were analyzed. Results. Significant differences were observed in mRNA and protein levels when compared with the NGT group, while methylation rates of eight CpG units within the FOSL2 gene were higher in the T2DM group. Methylation of CpG sites was found to inversely correlate with expression of other markers. Conclusions. Results show that a correlation between mRNA, protein, and DNA methylation of FOSL2 gene exists among T2DM patients from Uyghur. FOSL2 protein and mRNA were downregulated and the DNA became hypermethylated, all of which may be involved in T2DM pathogenesis in this population. [ABSTRACT FROM AUTHOR]

Studies have documented that unusually high expression of matrix metalloproteinase-9 (MMP-9) suppresses wound healing during the late stages of diabetic foot ulcers. Recently, it has been reported that the presence of advanced glycation end products-bovine serum albumin (AGE-BSA) resulted in a higher expression of MMP-9 in skin primary keratinocytes. The aim of the present study was to elucidate the molecular machinery that is responsible for the inappropriately high AGE-BSA-induced expression of MMP-9. It has been demonstrated that site-specific DNA demethylation played an important role in MMP-9 expression in AGE-BSA-stimulated keratinocytes. Ten-eleven translocation-2 (TET2) was up-regulated, whereas the percentage of methylation in the MMP-9 promoter was reduced. Furthermore, TET2 directly bound to a fragment surrounding the transcriptional start site in the MMP-9 promoter region, contributing to the regulation of MMP-9 expression. In addition, evidence indicated that TET2 affected the migration and proliferation in vitro of cultured skin primary keratinocytes. These findings indicated that TET2 directly interacted with the promoter region of MMP-9 in diabetic tissues and may be a novel master regulator of wound healing. [ABSTRACT FROM AUTHOR]

Soft tissue sarcomas (STSs) are a rare and fascinating group of diseases that can be subdivided into specific reciprocal translocations in STSs (SRTSs) and nonspecific reciprocal translocations in STSs (NRTSs). PTEN mutations are rare in STSs, suggesting that PTEN expression may be lost by alternative mechanisms such as methylation. In order to reveal whether aberrant PTEN methylation occurs in STSs, MassARRAY Spectrometry was carried to detect methylation patterns of PTEN in STSs. We evaluated methylation levels in 41 CpG sites from −2,515 to −2,186 bp (amplicon A) and −1,786 to −1,416 bp (amplicon B) relative to the translation initiation site in 110 different cases (46 cases of SRTSs, 40 cases of NRTSs, and 24 cases of normal controls). In addition, immunohistochemistry (IHC) was used to detect the loss of PTEN to determine whether PTEN alterations were responsible for decreased PTEN expression. Our data showed that expression of PTEN was diminished in 49 (57%) STSs, whereas the remaining cases (43%) were classified as high expression. Our previous results found that only 2 of 86 cases (2.3%) had a PTEN mutation suggesting that PTEN may be mainly downregulated in STSs by methylation, but not by mutation of PTEN itself. We observed that amplicon A was hypermethylated in STSs with low PTEN expression, whereas normal controls had low methylation levels (P<0.0001), which was not present in amplicon B (P>0.05), nor were there significant differences in the methylation levels in PTEN between SRTS and NRTS cases. The majority of individual CpG units within two amplicons was demonstrated to be hypermethylated. These findings indicate that PTEN hypermethylation is a common event in STSs suggesting that the inactivation of PTEN may be due to hypermethylation in the promoter of PTEN. The aberrant methylation of the CpG sites within PTEN promoter may serve as a potential candidate biomarker for STSs. [ABSTRACT FROM AUTHOR]

The article presents a study on the enhanced green fluorescent protein (EGFP) expression in transgenic chickens. The ability of the 2-(kilobyte) kb promoter fragment of the chicken ovalbumin gene to elicit tissue-specific expression of a foreign EGFP gene in chickens. The study projected potential of chicken ovalbumin promoter for the production of biologically active proteins in egg whites.

Abstract: Long non-coding RNAs (lncRNAs) are emerging as an integral functional component of human genome and have been investigated as critical regulators in molecular biology of cancer. A recent study reported that lncRNA-UCA1 induced drug resistance in adriamycin chemotherapy. However, the contributions of lncRNAs to adriamycin resistance in cancers remain largely unknown. To address this issue, we performed a genome-wide lncRNA microarray analysis in adriamycin resistant MCF-7/ADR and parental MCF-7 cells, and revealed differential expression of lncRNAs in distinct category and chromosome distribution patterns. A specific differentially expressed lncRNA (Adriamycin Resistance Associated, termed ARA) was validated in MCF-7/ADR and HepG2/ADR cells. ARA is derived from an intron of PAK3 gene, predicted to contain several stable hairpins in secondary structure and has conservative sequences in primates. ARA expression is significantly associated with adriamycin sensitivity in a panel of breast and liver cancer cell lines and is markedly up-regulated in parental sensitive MCF-7 and HepG2 cell lines after receiving adriamycin treatment. The functions of ARA were assessed by silencing this lncRNA in vitro, and we found that ARA knockdown reduced the proliferation, induced cell death, G2/M arrest and migration defects. Furthermore, microarray transcriptomic analysis was carried out to comprehensively depict the ARA-regulated genes. We showed that ARA can modulate multiple signalling pathways, including MAPK signalling pathway, metabolism pathways, cell cycle and cell adhesion-related biological pathways, and regulate cellular processes, including transcriptional processes and protein binding function. Overall, our results indicate novel insights of adriamycin resistance in lncRNA level. [Copyright &y& Elsevier]