Potential Role In Occurrence Research Articles

Peptidomic changes in human serous colorectal cancer patients.

Colorectal cancer (CRC) is the third most common cancer worldwide and one of the leading causes of cancer-related death. Peptidomics, considered a novel branch of proteomics, has an increasing range of applications in the screening, diagnosis, prognosis, and even monitoring of cancer. However, there is little information for peptidomics analysis in CRC. In this study, a comparative peptidomic profiling was analyzed in 3 CRC tissue samples and 3 adjacent intestinal epithelial tissue samples by liquid chromatography-tandem mass spectrometry (LC-MS/MS). Among the total 133 nonredundant peptides identified, 59 were significantly differentially expressed in the CRC samples and benign colonic epithelium conditions [fold change (FC) >2, P<0.05]. Totals of 25 up-regulated and 34 down-regulated peptides were detected, respectively. Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were applied to predict the possible functions of these relevant precursor proteins. To clearly identify the potential interaction network of peptide precursors, the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) was used to determine protein interactions and a possible central role in CRC. Our results for the first time revealed the differentially expressed peptides between the serous CRC tissue and the adjacent intestinal epithelial tissue samples, and these prominently variable peptides might have an important potential role in occurrence and development of CRC.

LncRNA SNHG1 alleviated apoptosis and inflammation during ischemic stroke by targeting miR-376a and modulating CBS/H2S pathway

Background Ischemic stroke (IS) is a major public health issue causing mortality and disability and is more difficult to treat than other cerebral diseases. Previous study reported that miR-376a was upregulated in the serum of stroke patients, indicating that miR-376a played potential role in occurrence and development of stroke. Methods IS cell model was induced by oxygen-glucose deprivation (OGD) exposed HCMEC/D3 cells. The mRNA level of SNHG1, miR-376a and inflammatory cytokines were detected by q-PCR. Protein level of CBS, apoptotic proteins were examined by Western blot. Apoptosis was analyzed by flow cytometry, and H2S level was measured by kit. Interaction among lncRNA, miRNA and target gene was validated by luciferase assay. Results Our research revealed that mRNA level of SNHG1 and CBS in HCMEC/D3 cells was downregulated while miR-376a was upregulated under OGD conditions. Further results demonstrated that miR-376a overexpression promoted apoptosis and inflammation while SNHG1 overexpressing alleviated such processes. Mechanistically, SNHG1 directly targeted miR-376a, and CBS was a target of miR-376a. Moreover, SNHG1 exert its function via inhibiting miR‐376a to regulate CBS expression. Conclusion LncRNA SNHG1 depressed apoptosis and inflammation of IS cell model via inhibiting miR-376a and upregulating CBS/H2S signal. These results show light on underlying mechanisms of IS and provide potential targets for IS therapy.