Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.12.2 (MEK)
 18,161 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastric carcinoma (GC) is one of the most common malignancies worldwide. To identify the candidate carcinoma-related biomarker in GC, comparative proteome technique was performed in resected GC tissues and matched adjacent non-cancerous gastric tissues (ANGT). As a result, S100A2 was successfully identified to be down-regulated significantly in GC compared with ANGT. Western blot analysis validated decreased expression of S100A2, and its expression level was related with the degree of tumor differentiation and status of lymph node metastasis in GC. Furthermore, immunohistochemistry analysis showed S100A2 down-expression was significantly associated with poor differentiation (P < 0.05), advanced depth of invasion (P < 0.05) and lymph node metastasis (P < 0.05) in GC. Kaplan-Meier curves showed that the relapse-free probability and the overall survival rate were significantly decreased with S100A2 expression decreasing (P < 0.05). Cox regression analysis indicated S100A2 down-expression was a negative independent prognostic biomarker for GC. A supplement of S100A2 protein by S100A2 expression vector significantly decreased the number of invaded cancer cells MGC-803. However, knockdown of S100A2 expression by siRNA interference compromised the invasion ability of MGC-803 cells. Moreover, S100A2 negatively regulated MEK/ERK signaling pathway, and activation of this signaling pathway by S100A2 down-regulation increased in vitro invasion of MGC-803 cells. In conclusion, this study demonstrated the clinical significance of S100A2 expression in GC, and loss of S100A2 expression contributes to GC development and progression. Therefore, the determination of S100A2 expression levels contributes to predict the outcome of GC patients.
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PMID:Clinical significance of S100A2 expression in gastric cancer. 2431 73

Background: Gastric carcinoma (GC) is a common malignant tumor. Recently, it has been found that long non-coding RNAs (lncRNAs) play important role in cancer. In this paper, we investigated the effects and mechanism of lncRNA GASL1 in GC cells. Methods: GASL1 level in GC cells was up-regulated via cell transfection. Cell proliferation, migration, invasion were detected by CCK-8, BrdU, Transwell assays and western blot. In addition, the regulation of GASL1 on microRNA (miR)-106a level was detected using RT-qPCR and the binding between GASL1 and miR-106a was confirmed by bioinformatic prediction and luciferase reporter assay. The effects of overexpressing miR-106a on GASL1-regulated GC cell behaviors were further explored. Moreover, western blot also was used to detect the pathway-related proteins. Results: Overexpression of GASL1 decreased the viability and BrdU levels. Meanwhile, CyclinD1 level was decreased while p53 and p21 levels were strengthened by overexpression of GASL1. On cell metastasis, up-regulation of GASL1 decreased cell migration, invasion and related proteins matrix metalloproteinase (MMP)-9 and Vimentin levels. Meanwhile, silencing GASL1 exerted opposite effects on GC cells. Moreover, GASL1 negatively regulated and targeted miR-106a. Up-regulation of miR-106a weakened the functions of GASL1 in cell proliferation and metastasis. Besides, GASL1 decreased the relate-protein levels of PI3K/AKT and ras/raf/MEK/ERK pathways while miR-106a weakened these changes. ConclusionGASL1 restrained GC cell proliferation and metastasis and blocked PI3K/AKT and ras/raf/MEK/ERK pathways by sponging miR-106a.
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PMID:Long non-coding RNA GASL1 restrains gastric carcinoma cell proliferation and metastasis by sponging microRNA-106a. 3289 6