ABSTRACT
Objective To investigate the expression alteration and significance of long non-coding RNA (lncRNA)by GWAS(Genome-wide association study)between Esophageal squamous cell carcinoma(ESCC)and its adjacent normal esophageal tissues. Methods lncRNA and mRNA differential expression in 6 pairs of ESCC and matched non-cancerous tissues were screened by microarray assay. The target genes were predicted. Finally , GO(Gene Ontology)and Pathway analysis was used for the further research of lncRNA. Results A total of 680 lncRNA and 1472mRNA were differentially expressed at more than two-fold change(P ≤ 0.05,with 161lncRNA and 653mRNA up-regulated,519lncRNA and 819mRNA down-regulated between ESCC and its adjacent normal esophageal tissues. Gene ontology and pathway analysis results suggested that the differentially expressed genes were involved in 11 pathways.Theyare potentially associated with esophageal squamous cell carcinoma ,including post-translational protein modification ,mucin type O-Glycan biosynthesis and sphingolipid metabolism pathways , which mainly related to the changes of molecular function ,cellular components and biological processes. Through cis and trans analysis,a total of 15 differentially expressed lncRNA had cis-and/or trans-regulated target genes in the database,with 13 lncRNA had cis-regulated target genes,3 lncRNA had trans-regulated target genes,and 1 lncRNA had both cis- and trans-regulated target genes. Conclusion Compared with adjacent normal tissues ,a large number of lncRNA were expressed differentially in ESCC in Xinjiang Han people.Aberrantly expressed lncRNA may play important roles in ESCC development and progression through some signaling pathways ,which are of great significance for further search of new targets for the diagnosis and treatment of ESCC.
ABSTRACT
Objective To analyze the correlation between miR-31 and ESCC in expression of miR-31 in the plasma of ESCC in Xinjiang Kazak and Han nationality patients. Methods The plasma samples were collected respectively from patients with ESCC in 20 cases and healthy subjects in 20 cases. The relatively expression of miR-31 was detected by real-time Q-PCR. Results The expression of miR-31 with ESCC were higher than those of the normal control group, which related to the degree of tumor differentiation in Kazak ESCC patients (P < 0.01); the levels of miR-31 relative expression in Kazak were higher than that of Han (P = 0.008, P = 0.027). Conclusion miR-31 may be involved in the occurrence of ESCC in Han and Kazak nationality. miR-31 might be another risk factor in high incidence of ESCC in Kazak than Han nationality.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the role of the PI3K/Akt signaling pathway in hydrogen sulfide-induced alterations in expression of collagen I and collagen III in hepatic stellate cells.</p><p><b>METHODS</b>In vitro cultured rat hepatic stellate cells (HSC-T6) were treated with hydrogen sulfide, or left untreated for use as controls, and divided into groups for treatment with different inhibitors for the various factors involved in the PI3K/Akt signaling pathway. Reverse transcription-PCR was used to measure Collagen I and collagen III mRNA expression. Western blotting was used to detect the protein expression of PI3K and p-Akt, which are upstream proteins of the PI3K/Akt pathway.</p><p><b>RESULTS</b>Compared with the untreated control cells, the hydrogen sulfide treated cells showed elevated expression of collagen I mRNA (F =14.635, P less than 0.05), collagen III mRNA (F =14.620, P less than 0.05), PI3K protein (F =26.672, P less than 0.05), and p-Akt (F =23.522, P less than 0.05). Compared to the cells treated with hydrogen sulfide alone, the cells treated with the various inhibitors showed lower expression of collagen I mRNA (F =14.635, P less than 0.05), collagen III mRNA (F=14.620, P less than 0.05), PI3K protein (F =26.672, P less than 0.05), and p-Akt protein (F =23.522, P less than 0.05).</p><p><b>CONCLUSION</b>Hydrogen sulfide can activate the PI3K/Akt pathway and elevate the expression of collagen I and collagen III in rat hepatic stellate cells.</p>